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(Chest. 2001;120:409-415.)
© 2001 American College of Chest Physicians

The Perception of Dyspnea in Patients With Mild Asthma*

Marc H. Lavietes, MD, FCCP; Jyoti Matta, MD; Lana A. Tiersky, MD; Benjamin H. Natelson, MD; Leonard Bielory, MD and Neil S. Cherniack, MD

* From the UMD-New Jersey Medical School, Division of Pulmonary Medicine (Drs. Lavietes, Matta, and Cherniack), Newark, NJ; Asthma and Allergy Research Center (Dr. Bielory), UMD-New Jersey Medical School, Newark, NJ; Chronic Fatigue Syndrome Research Center (Dr. Natelson), Veterans Administration Medical Center, Newark, NJ; and School of Psychology (Dr. Tiersky), Fairleigh Dickinson University, Hackensack, NJ.

Correspondence to: Marc H. Lavietes, MD, FCCP, UMD-New Jersey Medical School, University Hospital, I-354, 100 Bergen St, Newark, NJ 07103-2406


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Background: Airway function, as assessed by standard spirometry, and the intensity of dyspnea reported by asthmatic patients correlate poorly.

Objective: This study tests the following two hypotheses: (1) that measures of the tendency of a patient to somatize will reduce the variation in the report of dyspnea not explained by airway function; and (2) that plethysmography is a better tool with which to estimate the degree of dyspnea associated with asthma.

Design: A prospective laboratory study carried out over one study session.

Participants: Forty asthmatic subjects who had withheld bronchodilator (BD) therapy overnight.

Interventions: We performed spirometry, plethysmography, and an assessment of dyspnea (ie, modified Borg scale) on all subjects before and after they received BD therapy. Standard questionnaires pertaining to psychological state and trait were administered as well.

Results: The change in specific airway conductance with BD therapy correlated with a decline in the Borg score (r = 0.47; p = 0.007). By contrast, neither spirographic measures nor measures of static lung volumes correlated. Correlation with the Borg scale score was not improved by adding indexes of either somatization or psychological state or trait.

Conclusion: The relief of dyspnea reported by patients with mild asthma after BD therapy is related to dilatation of the central airways.

Key Words: asthma • dyspnea • psychophysiology • somatoform disorders


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
When asthmatic patients complain of dyspnea or chest tightness, their symptoms do not correlate well with the degree of their airway obstruction, as measured by spirometry.1 Although patients in stable condition with asthma always recognize an increase of dyspnea with the induction of bronchospasm, there is a wide range in the magnitude of dyspnea that these patients associate with a fixed decline (eg, 20%) in the FEV1.2 3 4

Both pathophysiologic and psychological factors have been proposed to explain this variability in the perception of the magnitude of dyspnea among asthmatic subjects. Asthmatic subjects whose airway pathology features inflammation and eosinophilia more than bronchospasm, for example, report less dyspnea with a given fall in FEV1 than do other asthmatic subjects whose obstruction is transient and readily reversible with bronchodilator (BD) treatment and whose sputum eosinophilia is low.5 6 This may be attributed to the prolonged period of adaptation associated with chronic progressive airway inflammation.

Two lines of observation suggest that psychological factors may influence symptom perception as well. First, it is known that asthmatic patients scoring high on a scale measuring defensiveness are less accurate than others in their psychophysical magnitude estimates of external, inspiratory resistive loads. These subjects also perform poorly when asked to judge the quality of respiratory sensations associated with loading. These data indicate that the link between load recognition and the report of dyspnea is weak, at least in subjects with certain psychological traits.7 A study of asthmatic children showed no correlation between the precision with which the child identified an external load and his or her sense of shortness of breath.8 A second line of observation holds that suggestion may play a role in the provocation of bronchospasm.9 10 For example, some subjects who are responsive to a given asthma trigger (eg, ragweed) will wheeze when presented with a photograph of a ragweed plant.

Tools are available to assess the tendency of an individual to "somaticize," that is, to exaggerate responses to benign impulses associated with normal physiologic function and, thus, to misconstrue these responses as symptoms of organic disease.11 A person’s tendency to somaticize is not related to any psychological state, trait, or psychiatric diagnosis.

This study tested the hypothesis that, in asthmatics, much of the variation in reports of dyspnea not explained by airway function might be explained by a variation in the tendency of individuals to somaticize. We asked asthmatic subjects to rate their degree of dyspnea and to perform lung function tests before and after bronchodilation. Subjects also responded to questionnaires designed to evaluate their tendency to somatize. Both spirometry and plethysmography were used to assess airway function. This allowed us to formulate and examine a second hypothesis, namely, that a plethysmographic measure of airway resistance rather than spirometry might best predict the magnitude of dyspnea (or the change in dyspnea associated with BD treatment) perceived by individual asthmatic subjects.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Subjects
Forty patients in stable condition (32 women and 8 men) with mild asthma were recruited from the outpatient asthma clinic. All patients on entering the clinic had demonstrated a >= 15% increase in FEV1 in response to an inhaled BD. The average (± SD) age was 40 ± 9 years. None had any other cardiopulmonary or psychiatric disorders. Patients receiving either psychotropic medications or recreational drugs were excluded from the study. The study was approved by the local institutional review board. All subjects signed informed consent forms.

Procedures
Lung Function Testing:
Spirometry, lung volume determinations, and plethysmographic measurements of airways resistance were performed with standard equipment (DSII plus; WE Collins; Braintree, MA).

The modified Borg scale was used to obtain quantitative assessments of dyspnea.12 At prescribed intervals, subjects were presented with the scale and were asked to rate the magnitude of their dyspnea in the following way. They were told that 0 represented no breathlessness at all while 10 represents the "strongest feeling of breathlessness you have ever known." Subjects then were asked to select either a number from 0 to 10 on the printed scale or an adjacent verbal descriptor that would represent their degree of breathlessness at that moment.13

Psychometric Evaluation:
Three tests of psychometric evaluation were used. The Barsky somatosensory amplification scale (SSAS) was used to assess the tendency to amplify symptoms.14 This 10-item questionnaire asks the subject to estimate the degree of discomfort that he or she would associate with each of 10 common but minor physical sensations, all of which are unlikely to reflect major abnormalities (eg, feeling hunger contractions). Second, sections of the revised Hopkins symptom checklist (SCL-90-R) were used to examine the following four symptom dimensions: somatization; psychoticism; anxiety; and depression.15 The SCL-90-R is a standard tool designed to measure psychopathology. Finally, the neuroticism subset of the personality inventory of Costa and McCrae16 was administered. Neuroticism, thought by Costa and McCrae to be the most pervasive facet of personality, is ranked for each subject on a range between emotionally stable and unstable or maladjusted.

Protocol:
Subjects refrained from using ß2-agonists for 12 h prior to the study. On reporting to the laboratory, they performed spirometry and plethysmography, and scored their dyspnea on the Borg scale. To avoid an effect on our data of the transient bronchoconstriction that may accompany a deep breath in asthma, the spirometry and plethysmography procedures were separated by 5 min.17 The first 30 subjects were told that they would receive BD therapy (ie, aerosolized albuterol) after first performing the tests and did inhale a BD. Over the next 20 min, psychometric questionnaires were administered. Then lung function measurements were repeated, and the Borg scale again was administered.

The protocol differed for the final 10 subjects in that they were told that they would receive either a BD or a placebo (namely, saline solution [SAL]), and in fact they received a nebulized SAL.

Data Analysis:
Standard equations from the literature were used to convert lung volumes given in liters to a percentage of a predicted value.18 Standard methods of data analysis included paired comparisons (paired t test) and regression analysis (ie, Pearson correlation coefficient and multiple stepwise analysis). The data for two of the subjects were incomplete, in that they provided acceptable data for lung function studies but did not complete the psychometric evaluation satisfactorily.

To evaluate the data from the 10 subjects in the SAL placebo-treated group, we formed a comparison subgroup from among the original 30 subjects. This comparison group was composed of 14 subjects whose change in Borg scale score was identical to that of the SAL-treated group (ie, <= 0.10 U).


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The first 30 subjects studied had minimal airway obstruction at the time of study (FEV1, 74 ± 26% of the predicted value). Three subjects were smokers. Six subjects had a history of previous hospitalization, but only one had ever been intubated. All were receiving inhaled adrenergic agonists, steroids, or both. Two subjects reported recent treatment with short courses of oral steroids. Lung function data recorded both before and after BD therapy for these subjects appear in Table 1 . The changes expected with treatment were reflected in all variables. Specific airway conductance (sGaw), for example, increased from 0.14 ± 0.11 sec-1 cmH2O-1 before BD use to 0.30 ± 0.23 sec-1 cmH2O-1 after treatment (paired t test, 4.93; p < 0.001). Correspondingly,the Borg scale score decreased from 3.2 ± 1.9 prior to therapy to 1.2 ± 1.1 after treatment (paired t test, 7.40; p < 0.001).


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  		Table 1. Lung Function Tests Before and After BD Administration (30 Subjects) *

 
No correlation was found between the Borg scale score obtained from all 30 subjects prior to BD therapy and any index of lung function measured prior to treatment. Similarly, no correlation was observed between the change in Borg scale score (pretherapy minus posttherapy) and any measure of pulmonary function made prior to therapy.

The changes in sGaw and Borg scale scores were highly correlated (r = 0.47; p = 0.007). Inspection of Figure 1 , however, shows a wide range of {Delta} Borg scale values in subjects showing little change in sGaw (eg, those whose sGaw values increased <= 0.10 U after therapy). By contrast, larger changes in airway function always were accompanied by a decrease in the Borg scale score. There were no significant correlations between other measures of lung function and Borg scale scores (Table 2 ).



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  		Figure 1. Correlation between the change in sGaw with BD therapy (posttherapy minus pretherapy) on the abscissa and the change in Borg scale score (pretherapy minus posttherapy) on the ordinate in 28 patients.

 

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  		Table 2. Relationship Between Change in Borg Responses Before and After BD Administration and Lung Function Measures *

 
No correlations were found between the Borg scale score prior to BD therapy and either any of the four symptom dimensions of the SCL-90-R or the neuroticism subset of Costa and McRae.16 There was a tendency toward correlation between somatization, as measured by the Barsky SSAS, and the change in Borg scale score with therapy (r = 0.337; p = 0.08). While there was significant correlation between the Barsky SSAS score and somatization as measured by the SCL-90-R (r = 0.43; p = 0.008), the latter measure did not correlate with the change in the Borg scale response. There were no correlations between either the measures for other dimensions of the SCL-90-R or neuroticism with the change in Borg scale score before and after BD administration. The addition of any psychometric index as a second independent variable did not improve the ability to predict the change in Borg scale score from the change in sGaw.

Response to Inhalation of Placebo
Lung function test results for the 10 SAL-treated subjects appear in Table 3 . The results for these subjects were similar to those for the first group studied. Two subjects had been hospitalized previously (one subject had been intubated previously), one subject currently smoked, and all subjects were receiving inhaled adrenergic or steroid preparations. Prior to SAL inhalation, the mean FEV1 values, as measured both in liters (1.84 L) and as percent predicted (66%), were no different from those for the first 30 study subjects. Similarly, the values for airway resistance and functional residual capacity (FRC) for the SAL-treated subjects were similar to those of the 30 subjects who had received BD treatment. No changes were observed in lung function after or before SAL inhalation in these 10 SAL-treated subjects.


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  		Table 3. Lung Function Tests Before and After BD Administration (10 SAL-Treated Subjects) *

 
The data presented in Table 4 show that the mean sGaw for the 10 SAL-treated subjects before therapy was 0.12 ± 0.13 L/cm H2O/s, and the corresponding Borg scale score was 2.3 ± 2.7. For the comparison BD-treated group, the initial sGaw was 0.13 ± 0.13 sec-1 cmH2O, and the initial Borg scale score was 2.7 ± 2.0. Note that descriptive data for this BD-treated group differ slightly from those values given in Table 1 . This is so because these data are taken from a subgroup of 14 subjects selected from the original group of 30 who are described in Table 1 . Values for the initial sGaw, the change in sGaw, and the initial Borg scale score did not differ between the SAL-treated and BD-treated groups. By contrast, the decrease in dyspnea experienced by many in the BD-treated group was great enough so that the overall change in Borg scale score in the BD-treated group (1.5 ± 1.4 U) was greater than that for the SAL-treated group (0.4 ± 1.2 U; unpaired t test, 2.34; p < 0.03). No differences were seen in the responses to somatization questionnaires between the SAL-treated and BD-treated groups.


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  		Table 4. Comparison of Lung Function and Borg Scale Responses to Therapy in BD-Treated vs SAL-Treated Groups

 
Correlation Analysis for Entire Study Group
Data for the 28 subjects who received BD and completed the full study were combined with the data from the 10 subjects who received placebo for analysis. Results were similar to those shown in Table 2 for the first group. The addition of the SAL-treated group did not improve the likelihood of correlation of either measure of somatization with change in the measure of any lung function.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Airway Function and Dyspnea
Most published studies, like this one, have found no correlation between the initial estimate of dyspnea of an asthmatic patient when presenting for treatment and FEV1.1 19 20 While one study21 did show such a correlation, the correlation coefficient (0.48) was such that only 25% of the variability in the Borg scale score was explained by the FEV1. Of interest, the mean FEV1 of subjects entering that study (24 ± 15% of predicted) describes subjects with severe airway obstruction. A relationship between the dyspnea index and FEV1 would be more easily observed in that patient group than in ours; larger changes in FEV1 following therapy would be demonstrated in that group composed of patients with greater bronchoconstriction than were our subjects. This is because the graphic relationship between a physiologic variable (eg, FEV1) and a psychosocial variable (eg, dyspnea) is often sigmoidal. A linear relationship between such variables would not likely occur when values for the independent variable (eg, FEV1) cluster at an extreme of the graph. To that end, the only publication20 that has found a correlation between the change in Borg scale score and the change in FEV1 for individual subjects studied asthmatic patients who presented to the emergency department for treatment. The FEV1 for those patients (35 ± 15% of predicted) rose to 50 ± 22% of predicted after therapy. Thus, values for the independent variable ranged from severe to moderate airway obstruction in that study. The correlation between the change in Borg scale score and the change in FEV1 , determined 30 min after treatment, nevertheless was poor (r = 0.28; p < 0.05).

Other authors have examined the relationship between airway function and dyspnea during the induction of bronchospasm. These studies have compared indexes of dyspnea rated first when the patient was in stable condition and rated again after the production of a 20% decline of FEV1 . Given these published data,22 it is possible that the change in FEV1 for our study group (10% of a predicted value) was too small to elicit a change in the perception of dyspnea in our subjects.

The decrease of Borg scale score without a concomitant change in FRC deserves comment. The elevation of FRC by 0.25 L in healthy subjects (which is similar to the change in FRC in our subjects) by positive end-expiratory pressure administered via a mouthpiece is associated with an increase of 1 U on the Borg scale.23 When, in another study,22 bronchoconstriction was induced in patients in stable condition with mild asthma, the change in end-expiratory lung volume rather than the change in airways resistance was the strongest predictor of change in the perception of dyspnea. Bronchodilation (ie, the opposite of bronchoconstriction) is accompanied by the withdrawal of the stimulus for dyspnea; that is, a lessening of the displacement of inspiratory muscles from their normal resting position occurs. Our data may differ from those of others cited in that in those studies the change in dyspnea was brought about by an increase, not a decrease, in airways resistance and lung volume. To our knowledge, however, there is no reason that the changes in the magnitude of dyspnea perceived by a subject should depend on the direction (eg, bronchoconstriction or bronchodilation) of the change in airway function.

Given the inability of a change in FEV1 to predict a change in Borg scale score in this study group, the correlation between the change in sGaw and the change in Borg scale score is of interest. Dynamic airway compression, a physiologic event that is reflected by the FVC maneuver, is thought to be important in the genesis of the sensation of dyspnea. It is unlikely, however, that patients whose FEV1 values exceed 60% of predicted would experience dynamic airway compression during quiet breathing.24 An alternate explanation for our findings might be that the magnitude of the sensation of dyspnea is related to the amplitude of the tidal swing of esophageal pressure.22 This measure of inspiratory pressure would clearly be related to airway conductance but not to FEV1 . The sensation of dyspnea during bronchospasm is mediated by afferent sensory airway receptors. These receptors would likely monitor changes in the tidal swing of esophageal pressure during quiet breathing.25 26 Our study supports the notion of Noseda et al27 that the sGaw measure is the most appropriate measure with which to predict the magnitude of the change of dyspnea accompanying a therapeutic intervention in asthmatic patients with mild airway obstruction.

Dyspnea and Indexes of Psychological State or Trait
Our data do not support the hypothesis that a measure of somatization will reduce the unexplained variability between any measure of airway function and the degree of dyspnea reported by asthmatic subjects. We used two somatization scales (the Barsky SSAS and the SCL-90-R) because the published data show poor correlation between these scales. Our correlation between the data derived from the two instruments (r = 0.43) is similar to that previously observed.28 This discrepancy between the two instruments is not unexpected. The Barsky SSAS is designed to assess the awareness of multiple somatic symptoms, while the SCL-90-R assesses the degree of physical discomfort associated with a symptom. Neither instrument served as a second independent variable with the change in sGaw to predict the change in Borg scale score. This observation is compatible with other data that show that there is poor correlation (R2 = 0.16) between a measure of hypochondriasis and disease severity in asthmatic subjects.4

Our study group was limited to ambulatory asthmatic patients in stable condition. Because our patients were recruited solely from an outpatient setting, patients with severe airway obstruction were excluded. Observations from other studies29 30 suggest that patients presenting with symptoms that are suggestive of any disease but with no objective findings of that disease are likely to score highly on any somatization scale, whereas patients with objective findings show less of a tendency to somaticize. In this regard, our subjects scored 2.9 ± 0.7 on the Barsky SSAS and 1.1 ± 0.7 on the SCL-90-R. This mean value of 2.9 on the Barsky SSAS would be associated with a high degree of somatization, and, by contrast, the mean value of 1.1 for the SCL-90-R would describe a population less likely to somaticize.15 31 These observations taken together raise the possibility that a wider range of Barsky SSAS scores would be observed if the study group were composed of patients with a greater range of airway function.

Placebo Effect of Albuterol
Our observation (Fig 1) that many subjects who did not demonstrate a large increase in sGaw with albuterol nevertheless reported a decrease in their Borg scale score prompted us to recruit 10 additional subjects to inhale isotonic SAL (placebo). This group of 10 was matched to 14 subjects from among the original 30 such that the two resultant groups had similar initial sGaw values and similar changes in sGaw with treatment. Table 4 shows that those in the original BD (albuterol)-treated group were more likely to report symptomatic relief, despite their lack of physiologic response, than those in the SAL-treated group. This in fact may have represented a placebo effect, in that subjects in the albuterol-treated group were told that they would be receiving a BD while subjects in the SAL-treated group were told that they would receive either BD or a placebo.32 An alternate possibility is that albuterol has some dyspnea-sparing effect beyond its effect as a BD. Selective ß2-agonists increase the concentrations of glucose, lactate, and free fatty acids in plasma.33 There is evidence that during submaximal exercise, partial ß2-agonist activity attenuates dyspnea when it has been exacerbated by generalized ß-blockade.34 A proposed mechanism for this is the increased fatty acid availability associated with ß-agonism and its resultant glycogen-sparing effect. Whether or not this mechanism would operate in this protocol when the patients are breathing at rest and the drug has been administered by aerosol is unknown.

In summary, this study showed that asthmatic patients with mild airway obstruction are likely to associate the relief of dyspnea with BD therapy. For those subjects whose sGaw level increases >= 0.1 U after bronchodilation, a linear relationship was seen between the magnitude of changes in conductance and Borg scale scores. By contrast, such a relationship was not seen between the change in dyspnea rating and the change in any spirometric measure of airway function. Some subjects whose sGaw levels increased minimally (<= 0.1 U) with bronchodilation nevertheless reported a decline in their dyspnea score; no subjects receiving placebo reported such a change. Psychophysiologic measures of somatization did not explain any variability between airway function and dyspnea rating.


   Acknowledgements
 
We thank Dr. Gloria Okoh for help with data collection and our laboratory technician, Ms. Gail Smith.


   Footnotes
 
Abbreviations: BD = bronchodilator; FRC = functional residual capacity; SAL = saline solution; SCL-90-R = Hopkins symptom check list; sGaw = specific airway conductance; SSAS = somatosensory amplification scale

Dr. Natelson is supported by National Institutes of Health Center grant U01A1–32247.

Received for publication April 10, 2000. Accepted for publication March 2, 2001.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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Listening to Our Patients
Chest, June 1, 2005; 127(6): 1877 - 1878.
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