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(Chest. 2003;124:2164-2170.)
© 2003 American College of Chest Physicians

Overall Contribution of Chest Wall Hyperinflation to Breathlessness in Asthma*

Mario Filippelli, MD; Roberto Duranti, MD; Francesco Gigliotti, MD; Roberto Bianchi, MD; Michele Grazzini, MD; Loredana Stendardi, MD and Giorgio Scano, MD, FCCP

* From the Department of Internal Medicine, Section of Respiratory Disease, University of Florence, and Fondazione Don C.Gnocchi, IRCCS, Pozzolatico, Florence, Italy.

Correspondence to: Giorgio Scano, MD, FCCP, Department of Internal Medicine, Section of Clinical Immunology, Allergology and Respiratory Disease, University of Florence, Viale Morgagni 87, 50134 Firenze, Italy; e-mail: g.scano{at}dmi.unifi.it


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Results
 References
 
Background: Studies suggest that the increased volume of both abdominal and rib cage compartments of the chest wall contribute to dyspnea during methacholine-induced airway narrowing.

Material: Eight male patients with asthma aged 34 ± 13 years (mean ± SD) before and during methacholine challenge.

Methods: The volume of the chest wall (Vcw), volume of the abdomen (Vab), and volume of the rib cage (Vrc) were measured by using a three-dimensional optoelectronic plethysmography.

Results: During methacholine challenge, the increase in end-expiratory Vcw (Vcw,ee) [0.55 ± 0.23 L, p < 0.001] was due to increased Vrc (0.37 ± 0.20 L, p < 0.01) and, to a lesser extent, Vab (0.18 ± 0.10 L, p < 0.005). Linear univariate regression analysis showed that changes in dyspnea (Borg scale) with the highest methacholine dose correlated with both {Delta}FEV1 and {Delta}Vcw,ee. Multiple regression analysis with the Borg score as dependent variable and all other ventilatory indexes as independent variables showed that {Delta}Vcw,ee and {Delta}FEV1 were the only significant contributors to the Borg score. Taken together Vcw,ee and FEV1 explained 56% of variance in the Borg score (r2 = 0.56), although Vcw,ee explained 48% of it.

Conclusions: During methacholine challenge in patients with asthma, the overall increase in Vcw,ee is a better predictor of dyspnea that the reduction in FEV1.

Key Words: asthma • chest wall • dyspnea • hyperinflation


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Results
 References
 
Dynamic hyperinflation (DH) during acute bronchoconstriction is an important determinant of breathlessness in patients with asthma.1 In such patients, however, the assessment of DH is problematic because measurements of the functional residual capacity (FRC) obtained with the gas-dilution methods may not be valid because of gas trapping, and the body plethysmographic method may overestimate the FRC because the increased airway resistance may delay the transmission of alveolar pressure to the mouth.2 The indirect method for assessing DH based on measurement of the inspiratory capacity is also questionable because with bronchoconstriction the total lung capacity may be reduced. A useful alternative is provided by a new noninvasive method, optoelectronic plethysmography (OEP), which estimates both the overall volume of the chest wall (Vcw) and that of its components, volume of the rib cage (Vrc) and volume of the abdomen (Vab).3 4 5 6 Such partitioning may also be useful to detect possible distortions of the chest wall during bronchial challenge. In fact, it has been shown that expiratory flow limitation, which promotes DH, is predominant in the dependent lung regions after methacholine challenge in asthmatics.7

Accordingly, in the present study we have used the OEP method in patients with asthma subjected to an methacholine challenge, in order to assess the role of the increased Vcw and its two compartments on breathlessness (Borg scale). The contribution of FEV1 and other lung function measurements on dyspnea was also assessed.


   Materials and Methods
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 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Results
 References
 
Patients
Eight clinically stable, male, asthmatic patients aged 20 to 59 years with chronic bronchial asthma according to the criteria of the National Heart, Lung, and Blood Institute8 participated in the study. Asthma was characterized by a history of episodes of dyspnea with wheezing and by bronchial hyperresponsiveness to methacholine, the provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) being < 8 mg/mL in all patients. No patients had received theophylline or oral corticosteroids in the last 6 months. Bronchodilators were withheld for at least 12 h before the study. All subjects had been free from acute respiratory infections within the preceding 8 weeks, and none had a history of smoking. Informed consent was given by each subject, and the study was approved by the local ethics committee.

Measurements
All patients were studied while sitting in an armchair with their forearms supported comfortably below the shoulder. Each patient breathed through a mouthpiece, wearing a nose clip. Spirometry was performed according to standard techniques using a water-sealed spirometer (Godart; Bilthoven, the Netherlands). FRC was measured by helium-dilution technique. Predicted values for lung function variables are those proposed by the European Community for Coal and Steel.9 Airflow was measured with a No. 3 Fleisch pneumotachograph, and the flow signal was integrated to give volume. The dead space of the mouthpiece and pneumotachograph was 70 mL, and the equipment resistance was 0.92 cm H2O/L/s.

Chest Wall Kinematics and Compartment Volumes
The Vcw was modeled as the sum of the Vrc and Vab.10 These volumes were assessed using the noninvasive OEP technique, previously described in detail.3 Briefly, 89 reflecting markers were placed in front and back over the trunk from the clavicles to the anterior superior iliac spines along predefined vertical and horizontal lines. Each marker was tracked in three dimensions by four videotape recording cameras. To measure the Vcw compartments from the surface markers, in line with Kenyon and co-workers,11 we defined the following: (1) the boundaries of rib cage (RC) as extending from the clavicles to the costal margin anteriorly down from the xiphisternum, and to the level of the lowest point of the lower costal margin posteriorly; and (2) the boundaries of the abdomen as extending caudally from the lower RC to a horizontal line at the level of the anterior superior iliac spine. The anatomic placement of the markers and the boundaries between chest wall compartments are shown in Figure 1 . The coordinates of the landmarks were measured with a system configuration of four infrared television cameras, two placed 4 m behind and two placed 4 m in front of the subject at a sampling rate of 50 Hz. Starting from these coordinates, the Vcw was computed by triangulating the surface and then using Gauss’s theorem to convert the volume integral to an integral over this surface, as described previously.3 The arrangement of the chosen markers and the geometric model allow the computation of the contribution of RC and abdomen to DH and tidal volume (VT). End-expiratory and end-inspiratory volumes of each compartment were measured at the beginning and end of inspiratory flow (zero-flow points). The difference between the end-inspiratory and end-expiratory volumes of each compartment was calculated as the VT contribution by each compartment. Thus, the Vcw was calculated as Vcw = Vrc + Vab, and changes ({Delta}) in Vcw were calculated as {Delta}Vcw = {Delta}Vrc + {Delta}Vab.



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  		Figure 1. Placement of 89 small (6 mm) passive reflective markers on the chest wall (42 anteriorly, 37 posteriorly, and 10 laterally). The markers were arranged in seven horizontal rows between the clavicles and the anterior superior iliac spines, five vertical rows both anteriorly and posteriorly, and one vertical row bilaterally in the mid-axillary line. The lines indicate the boundaries between the RC and abdomen.

 
The OEP calculates absolute volumes, and the absolute volume of each compartment at FRC in control conditions was considered as the reference volume. Volumes are reported either as absolute values or as changes from the volume at FRC in control conditions. We assumed that the measured {Delta}Vcw values were due entirely to changes in thoracic gas volume.

Bronchial Challenge
Each patient was administered a methacholine aerosol inhalation test according to a standardized procedure.12 Increasing concentrations of methacholine in normal phosphate-buffered saline solution were inhaled from a DeVilbiss 646 nebulizer (DeVilbiss; Somerset, PA), with an output of 0.13 mL/min. With this method, 4 mL of solution was placed in the nebulizer, and inhalation continued during tidal breathing for 2 min. The methacholine solution was stored at 4°C and was nebulized at room temperature. Normal phosphate-buffered saline solution was inhaled first, followed at 5-min intervals by methacholine in twofold-increasing concentrations from 0.016 to 8 mg/mL. The arterial oxygen saturation was monitored using an ear oximeter (Radiometer; Copenhagen, Denmark). Methacholine administration was discontinued when the following criteria were met: a fall in FEV1 > 40% of control, a plateau in FEV1 (< 5% change in FEV1 over two or more steps), and discomfort or breathlessness sufficient to induce the patient to interrupt the test. The test was also interrupted when the FEV1 reached approximated 40% of the predicted value. FEV1 was measured 1 to 1.5 min after the onset of inhalation of each methacholine concentration. Two measurements of FEV1 were performed, and the best value was used. From the log dose-response curve, the PC20 was noted. The log cumulative dose of methacholine was also calculated for each subject.

Dyspnea
The perception of breathlessness during the challenge test was with the Borg 0 to 10 scale13 before FEV1 measurements. Dyspnea was described to the patients as nonspecific discomfort associated with the act of breathing. The sensation of respiratory discomfort was referred to that felt by the subject during a previous asthma attack. The subjects were instructed that 0 signified no sensation at all, and that 10 signified the most severe sensation that they could imagine.

Protocol
Before the experiments, each subject was familiarized with the laboratory and equipment. Lung function tests were performed first. Vcw, Vrc, and Vab, along with flow and volume signals from the pneumotachograph, were recorded during a 2-min period of quiet breathing (baseline) and a 1-min period, 2 min after each methacholine concentration was administered. In each case, these measurements were followed by assessment of inspiratory capacity and FEV1. The baseline measurements of ventilation after each methacholine administration were averaged over 2 min. At the end of these experiments, albuterol was administered by nebulization. A physician not involved in the study was present throughout the study to take care of the patients.

Data Analysis
Values are means ± SD. A nonparametric statistical procedure was used to test differences (Wilcoxon test for paired samples). Individual regression analysis was performed using Pearson correlation coefficient. Least-square linear regression analysis was used to analyze the individual relationship between Borg scale as dependent variable and the concurrent reduction in FEV1, expressed as percentage of post-saline solution, and increase in end-expiratory Vcw (Vcw,ee), expressed in liters. Anthropometric characteristics, symptom score, baseline spirometry, breathing pattern (ventilation, VT, and respiratory frequency) and PC20 were analyzed as possible covariates. The level of significance was set at p < 0.05. When appropriate, multiple regression analysis with stepwise selection of the independent variables was carried out relating Borg score to functional variables. The proportion of total variance in the dependent variable, accounted for by the independent variables, is reported as the square of the correlation coefficient (r2). All statistical procedures were carried out using the Statgraphics Plus 5.0 statistical package (Manugistics; Rockville, MD).


   Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Results
References
 
Spirometric values at baseline were in the normal range (Table 1 ). At maximal bronchoconstriction, FEV1 decreased by 35% ± 15% from saline solution; in two subjects, the final doubling concentration of methacholine resulted in a marked FEV1 fall (approximately 50%) relative to that at the previous concentration. The Borg score increased by 4.4 ± 1.9 arbitrary units (au), Vcw,ee increased by 0.55 ± 0.23 L, end-expiratory Vrc (Vrc,ee) by 0.37 ± 0.20 L, end-expiratory Vab (Vab,ee) by 0.18 ± 0.10 L, and Vab,ee(%Vcw,ee) by 36.7 ± 26.6 (Table 2 ). All changes were significant (p < 0.01 to p < 0.001). Breathing pattern variables at maximal constriction relative to saline solution did not consistently change (Table 2) .


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  		Table 1. Demographic and Functional Characteristics of Eight Patients Under Control Conditions*

 

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  		Table 2. FEV1, Borg Score, Breathing Pattern Variables, and Vcw,ee, Vrc,ee, and Vab,ee at Maximal Bronchoconstriction*

 
Individual Regressions
Representative regressions of changes in the Borg score to changes in both FEV1 and Vcw,ee, expressed relative to FRC saline solution, and of changes in FEV1 to change in Vcw,ee are shown in Figure 2 . Table 3 shows the individual linear regressions of {Delta}Vcw,ee to {Delta}FEV1 (p < 0.03 to p < 0.01) and of {Delta}Borg to both {Delta}FEV1 (p < 0.02 to p < 0.01) and {Delta}Vcw,ee (p < 0.05 to p < 0.003). In subject 5, regression coefficients (r) were < 0.5. The individual Vab,ee to Vcw,ee ratios were fixed (Table 4 ), indicating that {Delta}Vab,ee (and by implication {Delta}Vrc,ee) are surrogate markers of {Delta}Vcw,ee. However, the {Delta}Vcw,ee/{Delta}Borg slopes did not correlate significantly to Vab,ee/Vcw,ee ratio (p > 0.1).



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  		Figure 2. Linear regressions of changes in the Borg score vs changes in FEV1 (left, A) and Vcw,ee (center, B), and of changes in FEV1 to changes in Vcw,ee (right, C). All experimental data points in a representative subject are shown during methacholine-induced bronchoconstriction. The changes in Vcw,ee are expressed relative to FRC saline solution.

 

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  		Table 3. Individual Regression Values of {Delta}Vcw,ee/{Delta}FEV1, {Delta}Borg/{Delta}FEV1, and {Delta}Borg/{Delta}Vcw,ee

 

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  		Table 4. Individual Vab,ee/Vcw,ee Ratio During Methacholine Inhalation

 
Overall Regression Analysis
Taken together, {Delta}Vcw,ee (r2 = 0.48) and {Delta}FEV1 (r2 = 0.08) explained 56% of the variance in the Borg score during methacholine challenge. After adjustment for {Delta}FEV1, the change in {Delta}Vcw,ee explained, as before, 48% of the variability in the Borg score. Both {Delta}Vrc,ee and {Delta}Vab,ee correlated significantly with the Borg score and, taken together, continued to explain 47% of the variance in the Borg score.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Results
 References
 
We have shown that in patients with asthma, the increase in Vcw,ee was the best predictor of changes in the Borg score during methacholine challenge. This volume increase involved both the RC and abdominal compartments.

Criticisms of Methods
We have previously reported that the VT measured by OEP closely reflected the VT measured by a pneumotachograph both under baseline conditions and during inhalation of histamine, the error of OEP in estimating VT being always < 4%.4 The assessment of the abdominal and RC compartments in the present study was based on external boundaries that may result in an underestimation of the absolute RC dimensions at end-expiration, when the diaphragm is displaced downward after methacholine. However, the diaphragm displacement was insufficient to increase the end-inspiratory abdominal volume ({Delta} end-inspiratory abdominal volume = 0.01 ± 0.03 L, p = not significant) and to qualitatively affect our results.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Results
References
 
Linear regression analysis showed that breathlessness was more strongly related to Vcw,ee than FEV1 or to other ventilatory parameters. Furthermore, after accounting for the change in FEV1, the changes in Vcw,ee were still closely correlated to breathlessness. In fact, after correction for FEV1, r2 did not change, indicating that the increase in perceived breathlessness intensity was better explained by the level of lung hyperinflation. These data are in line with previous studies showing that dynamic hyperinflation mainly accounts for intersubject variability in breathlessness both in patients with asthma1 and patients with COPD.14 The marked intersubject variability of slopes and intercepts (Table 3) may reflect the wide variation in the perception of breathlessness present in normal subjects, in whom the experience of breathlessness may modify subsequent estimates of breathlessness.15 In the presence of disease, it may not be possible to identify these inherent interindividual differences, and this may confound attempts to identify the effects of the disease.

The role of the RC and the abdomen has been analyzed by plotting Vab,ee against Vcw,ee. The individual correlations were highly significant and, in any given individual, the Vab,ee/Vcw,ee ratio was fixed (Table 4) , suggesting that {Delta}Vab,ee, and by implications {Delta}Vrc,ee, are surrogate markers of {Delta}Vcw,ee.

Although the mechanism(s) responsible for the marked interindividual differences in the contribution of {Delta}Vab to {Delta}Vcw (Table 2) are not fully understood, the following scenario might be considered: decreasing Vab,ee may be viewed as a mean to utilize the most compliant compartment to minimize the elastic work of moving the chest wall. Increasing the contribution of the abdomen to VT permits the elastic work of breathing to be shared between inspiratory and expiratory muscles.16 On this basis, one could explain why some subjects reduced Vab to a greater extent than others. In other words, volume responses may be to some extent determined by appropriate RC responses or abdominal responses.

We have previously shown that histamine-induced bronchoconstriction resulted in a significant increase in Vcw,ee, which was due to increased Vrc, whereas abdominal muscle recruitment during expiration limited the increase in the Vab.4 Several reasons may account for the different results obtained in the present study: (1) the inconsistent increase in Vab with histamine; two of our patients exhibited < 100 mL decrease and one patient exhibited > 500 mL increase; (2) the different study conditions (the agonists employed); and (3) the different clinical conditions of patients (eg, duration of disease, pharmacologic treatment, outcomes of airway inflammation).

What is the explanation for the contribution to breathlessness of increase in Vab,ee? It is likely that dynamic mechanisms of lung hyperinflation were operating at the airway level, delaying passive expiration and impeding lung regions to reach their relaxation volume during the time available for expiration.17 18 An increase of emptying time constant, and the occurrence of local airflow limitation with methacholine may retard regional lung emptying or trigger premature termination of expiration,19 thus resulting in hyperinflation in the subtending lung regions. Pellegrino et al7 showed that expiratory flow limitation occurred quite homogeneously across the chest wall compartments though airway closure was predominant in the dependent lung regions after methacholine in asthmatics. We believe that two mechanisms, DH and dynamic compression of the airway, contributed to breathlessness. DH affects breathlessness by putting the respiratory muscles in a disadvantageous portion of their length-tension relationship,4 such that a greater central respiratory output is required to maintain a given ventilation.20 The greater central output is perceived as a sense of effort that contributes to dyspnea.21 Furthermore, as DH imposes a load on the respiratory muscles and limits the VT, a greater inspiratory output for a given VT is required, that is, a neuromechanical dissociation of the ventilatory pump may result.1 However, dynamic compression of the airways may contribute per se to dyspnea: airway distortion and collapse due to dynamic compression may be a source of dyspnea via indirect or direct mechanisms22 23 24 ; these investigators stressed the influence of vagal irritant receptors on the discomfort associated with bronchoconstriction. Stimulation of vagal afferents also appears to intensify the sensation of breathlessness25 26 and may impart a sense of chest tightness or constriction.24

In turn, airway narrowing and lung hyperinflation are both involved in the perception of dyspnea.1 24 Application of OEP could allow us to define the effect of methacholine on breathlessness when the chest volumes are held constant. It could also help defining the way in which continuous positive airway pressure may result in breathlessness in healthy subjects or may decrease breathlessness in asthma.1 In summary, these data indicate that the overall increase in Vcw is related to the perception of breathlessness during methacholine challenge in patients with asthma.


   Footnotes
 
Abbreviations: au = arbitrary unit; DH = dynamic hyperinflation; FRC = functional residual capacity; OEP = optoelectronic plethysmography; PC20 = provocative concentration of methacholine causing a 20% fall in FEV1; RC = rib cage; Vab = volume of the abdomen; Vab,ee = end-expiratory volume of the abdomen; Vcw = volume of the chest wall; Vcw,ee = end-expiratory volume of the chest wall; Vrc = volume of the rib cage; Vrc,ee = end-expiratory volume of the rib cage; VT = tidal volume

Received for publication January 3, 2003. Accepted for publication June 18, 2003.


   References
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Results
 References
 

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