research article the interpretation of dyspnea in the

Research ArticleThe Interpretation of Dyspnea in the Patient with Asthma

Marc H. Lavietes

New Jersey Medical School, 100 Bergen Street, No. I354, Rutgers, Newark, NJ 07103, USA

Correspondence should be addressed to Marc H. Lavietes; [email protected]

Received 27 October 2015; Accepted 6 December 2015

Academic Editor: Andrew Sandford

Copyright © 2015 Marc H. Lavietes. This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Physicians have noted dyspnea in severely ill asthmatic patients to be associatedwith fright or panic; inmore stable patients dyspneamay reflect characteristics including lung function, personality and behavioral traits. This study evaluates the symptom of dyspneain 32 asthmatic patients twice: first when acutely ill and again after an initial response to therapy. Spirometry was performed,dyspnea quantified (Borg scale), and panic assessed with a specialized measure of acute panic (the acute panic inventory (API)) inthe 32 patients before and again after treatment. After treatment, questionnaires to evaluate somatization and panic disorder werealso administered.When acutely ill, both the API and all spirometric measures (PEFR; FEV1; IC) correlated with dyspnea. Multiplelinear regression showed that measures of the API, the peak expiratory flow rate, and female sex taken together accounted for 41%of dyspnea in acute asthma. After treatment, the API again predicted dyspnea while spirometric data did not. Those subjects whodescribed themselves as having chronic panic disorder reported high grades of dyspnea after treatment also. We conclude thatinterpretations of the self-report of asthma differ between acutely ill and stable asthmatic patients.

1. Introduction

Dyspnea is a cardinal symptom of asthma. The notion thatfear or panic may contribute to the sensation of dyspneaaccompanying acute bronchospasm has been recognized byclinicians and is discussed in the psychiatric literature [1].Similarly, physicians caring for outpatient asthmatics havelong recognized that both personality traits and psychologicalstate as well as pulmonary dysfunction may influence theself-report of dyspnea in stable patients [2–4]. This studyexamines the following hypothesis: the genesis of dyspneaexperienced by acutely ill asthmatic patients and that of stableasthmatic patients may differ.

2. Materials and Methods

We studied 32 English-speaking acutely ill asthmatic patientstwice: once immediately upon their arrival in the emergencyroom and again after stabilization. Subjects older than 50years or younger than 18 were excluded as were pregnantwomen and those with coexisting chronic heart or lungdisease.

Spirometry was first performed upon arrival at theemergency service before administration of any therapy. Weused a pneumotachograph affixed to a portable computer(Respitech, Lancaster, Pa). The procedure was repeated (asmany as six times) until reproducible expiratory flow andinspiratory capacity measures were obtained. Acceptableforced vital capacity measurements could not be obtainedfrom many subjects with severe airway obstruction and arethus not reported. Dyspnea was assessed with the modifiedBorg scale [5]. Patients were specifically asked to rank “howmuch discomfort do you feel with your breathing” on the zerothrough ten scale. Finally the 17-item acute panic inventory(API), a concise validated screening tool for panic, wasadministered [6]. Item number five of this inventory focusesspecifically upon dyspnea and was thus omitted from theinventory as used in this study [6, 7].

When stable (as promptly as within 2 hours of presen-tation in some cases but many days later in others) patientsreviewed and signed a consent form. Both the protocol inits entirety and the form were approved by our InstitutionalReview Board. This form encompassed both the initial andfollow-up studies. In addition to repeating the three tests

Hindawi Publishing CorporationPulmonary MedicineVolume 2015, Article ID 869673, 4 pageshttp://dx.doi.org/10.1155/2015/869673

2 Pulmonary Medicine

performed in the emergency room, subjects completed twoadditional questionnaires: one: the Barsky somatosensoryamplification scale (SSAS), a test of somatization [8]; two:the Spitzer binary assessment (SPTZ) (Y/N) for a clinicaldiagnosis of panic disorder [9].

We computed from the spirometry tracing peak expi-ratory flow rate (PEFR), forced expiratory volume in onesecond (FEV1), and inspiratory capacity (IC). Data withnormal distributions are presented as means and standarddeviations. Data with skewed distributions are presented asthree values: medians and both upper and lower extremes.Bivariate regression analysis was performed with a nonpara-metric method. Multiple linear regression was then usedto evaluate predictors of the Borg scale jointly. We usedstepwise, forward, backward, and Mallows’ Cp selectionmethods to construct a parsimonious model. All methodsyielded the same model. Since age and BMI were consideredpotential confounders and had not been selected via themodel selection procedure, they were added to the finalmodel. Categorical variables were compared with a one-wayanalysis of variance. Finally data obtained upon entrance tothe study were compared with data obtained at follow-up bypaired 𝑡-test. The SAS 9.3 statistical package was used. Alltesting was two-sided at the 0.05 significance level.

3. Results and Discussion

We studied 18 M and 14 F subjects. Their mean (SD) age was38 ± 7; their weight (BMI) was 30 ± 9 kg/m2. Their medianinitial Borg score was 5.0 (0.5; 8.0). Initial lung function datashowing severe airway obstruction appear in Table 1. Lungfunctions and their correlations with dyspnea during acuteillness appear in Table 1 also. Measures of all lung functionsas well as panic (API) correlated closely with acute dyspnea.Note that only 6 of the 32 subjects responded “yes” regarding apositive clinical history of panic attacks. Borg scale scores for“yes” and “no” responders were similar. The best fit multiplelinear regression model appears in Table 2. Spearman’s 𝑟for this model was 0.64. Measures of PEFR and API takentogether with the categorical variable sex accounted for 41%of the variability within the Borg scale response. While sexwas not predictive of dyspnea in the bivariate analysis, it wasin the multivariable analysis with women having higher Borgscores than men.

The median Borg score after treatment was 1 (0, 7). Thedifferences between pre- and postvalues for the API and alllung functions (Tables 1 and 3) were significant at the 𝑝 <0.001 level. Correlations of dyspnea measured after treat-ment with independent variables appear in Table 3. Lungfunction and dyspnea did not correlate. Both the API andthe binary assessment for the clinical diagnosis of paniccorrelated with dyspnea in the stable subjects. By contrast,correlation between dyspnea and either the SSAS or the BMIdid not reach statistical significance. Only the API howevercorrelated with dyspnea when all variables were entered intothe multiple linear regression model.

Dyspnea in acute asthma reflects both uncoupling ofinspiratory effort from inspiratory flow (airway narrowing)and hyperinflation. Both uncoupling and hyperinflation are

Table 1: Bivariate analysis using Spearman correlation to measureassociation of dyspnea (dependent variable) with lung functionand psychometric data obtained in the emergency department(independent variables) obtained simultaneously.

Independent variable Mean (+SD) Spearman 𝑟 𝑝

FEV1, % predicted 41 + 22 −0.47 0.006IC, % predicted 57 + 27 −0.37 0.036PEFR, % predicted 38 + 23 −0.45 0.009API 9 (1, 32) 0.55 0.001SPTZ 0.16 0.370API = acute panic inventory; FEV1 = forced expiratory volume, one second;PEFR = peak expiratory flow rate; IC = inspiratory capacity; SPTZ =Spitzer binary assessment, administered after treatment only. Group data forAPI scores are expressed as median (maximum, minimum). For all othervariables, group data are expressed as mean + SD.

Table 2:Multiple linear regressionmodel to predict correlationwiththe Borg scale score.

Characteristic Parameter estimate 95% CI 𝑝

Intercept 5.45 (2.24, 8.67)Sex (M/F) 1.88 (0.59, 3.17) 0.01Age −0.03 (−0.09, 0.02) 0.24BMI (kg/m2) 0.01 (−0.05, 0.07) 0.75PEFR, % predicted −0.05 (−0.08, −0.03) <0.001API 0.11 (0.06, 0.16) <0.001For definition of abbreviations, see Table 1.

Table 3: Bivariate analysis, data obtained after treatment, whenstable.

Independent variable Mean (+SD) Spearman 𝑟 𝑝

FEV1, % predicted 65 + 24 0.11 0.561IC, % predicted 87 + 22 0.04 0.821PEFR, % predicted 58 + 25 −0.01 0.979API 2 (0, 21) 0.59 0.004SPTZ 6 Y/26 N 0.53 0.002For definition of abbreviations, see Table 1.

promptly relieved by treatment. Subsequently in stable sub-jects, lung function is no longer a major determinant ofdyspnea.

Anxiety, as measured by the API, is a major determinantof dyspnea in the acutely ill subject. As such it is likely to be acomponent of acute panic.TheAPI is a simple, brief screeningtool designed to evaluate anxiety in severely ill, unstablesubjects. To this end, some of our patients when acutelyill resembled panic disorder patients. Many reported diffi-culty working, speaking, and concentrating. Some describedsweatiness and shaking. Two reported extreme symptomssuch as the need to urinate or defecate. It is likely that anoccasional patient presents with both severe bronchocon-striction and panic, too agitated to participate in a study. Wedid not encounter such a patient.The fact that only 6 subjectsresponded “yes” regarding a positive clinical history of panic

Pulmonary Medicine 3

and that this “yes” response was not linked to high Borgscores in the emergency setting suggests that panic disorderper se is not common in these patients and plays no role intheir dyspnea during acute illness.

The API as a measure of anxiety remained a strongpredictor of dyspnea after treatment. In addition, panicdisorder as assessed by the SPTZ questionnaire correlatedwith dyspnea when dyspnea was measured after treatment.The observation that the SPTZ correlates with dyspnea inthe treated but not the acutely ill asthmatic patient is ofinterest. The SPTZ is not a definitive diagnostic tool. It isa self-assessment screening tool that identifies patients whobelieve they qualify for the diagnosis of panic. In the contextof this study, the SPTZ identifies patients who see themselvesas being emotionally labile and, as such, would be likelyto exaggerate unpleasant sensations such as dyspnea. Takentogether, these data support two notions: one: the panicexperienced in acute asthma does not necessarily reflect ageneralized panic disorder; two: the mechanisms producingdyspnea in acute versus stable asthma differ.

Note that preexisting psychological conditions may pre-dispose to asthma or perpetuate the condition. This studydoes not address preexisting psychological conditions butsupports the notion that only panic and airway obstructionaccount for the dyspnea reported during an acute, untreatedasthma attack. By contrast, other psychological factors, notexamined here, may be more important in determining thedegree of dyspnea in the stabilized asthmatic patient [10–12].Lastly sex differences in exertional dyspnea, noted previously,are explained by differences in respiratory reserve betweenmen and women [13].

3.1. Limitations ofThis Study. This study population is limitedto inner city patients. The absence of suburban and ruralsubjects or subjects with varied socioeconomic and ethnicbackgrounds is amajor limitation to a generalized interpreta-tion of the results. Both cultural differences in the perceptionof symptoms and varied accessibility to health care betweenpersons of differing socioeconomic backgrounds are wellknown [14, 15]. Lastly a measure of airway inflammation,known to modify dyspnea perception in asthma but notobtainedhere, could have enhanced the prediction of dyspneain our subjects [16].

4. Conclusion

We conclude that the self-report of dyspnea and spirometryobtained simultaneously provide complementary informa-tion for the routine assessment of stable asthmatic patients.

Disclosure

The author is responsible for the content and writing of thepaper.

Conflict of Interests

The author reports no conflict of interests.

Acknowledgments

The author thanks Dr. Soyeon Kim for her assistance withthe statistical analysis and Dr. Norma MT Braun and Dr.MonroeKaretzky for critical reviewof the final paper.Dr.NeilCherniack played an integral role in the development of thisproject but passed away before its completion.

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[4] A. Chetta, G. Gerra, A. Foresi et al., “Personality profiles andbreathlessness perception in outpatients with different gradingsof asthma,” American Journal of Respiratory and Critical CareMedicine, vol. 157, no. 1, pp. 116–122, 1998.

[5] T. D. Bradley, D. A. Chartrand, J. W. Fitting, K. J. Killian,and A. Grassino, “The relation of inspiratory effort sensationto fatiguing patterns of the diaphragm,” American Review ofRespiratory Disease, vol. 134, no. 6, pp. 1119–1124, 1986.

[6] M. Sajatovic and L. F. Ramirez, Rating Scales in Mental Health,Lexi-Comp, Hudson, Ohio, USA, 2001.

[7] D. J. Dillon, J. M. Gorman, M. R. Liebowitz, A. J. Fyer, and D.F. Klein, “Measurement of lactate-induced panic and anxiety,”Psychiatry Research, vol. 20, no. 2, pp. 97–105, 1987.

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[10] J. W. Smoller, M. H. Pollack, M. W. Otto, J. F. Rosenbaum, andR. L. Kradin, “Panic anxiety, dyspnea, and respiratory disease.Theoretical and clinical considerations,” American Journal ofRespiratory and Critical Care Medicine, vol. 154, no. 1, pp. 6–17,1996.

[11] W. M. Brunner, P. J. Schreiner, A. Sood, and D. R. Jacobs,“Depression and risk of incident asthma in adults: the CAR-DIA study,” American Journal of Respiratory and Critical CareMedicine, vol. 189, no. 9, pp. 1044–1051, 2014.

[12] F. DiMarco, P. Santus, and S. Centanni, “Anxiety and depressionin asthma,” Current Opinion in Pulmonary Medicine, vol. 17, no.1, pp. 39–44, 2011.

[13] J. A. Guenette, D. Jensen, K. A. Webb, D. Ofir, N. Raghavan,and D. E. O’Donnell, “Sex differences in exertional dyspnea inpatients with mild COPD: physiological mechanisms,” Respira-tory Physiology and Neurobiology, vol. 177, no. 3, pp. 218–227,2011.

[14] G. K. Fritz, E. L. McQuaid, S. J. Kopel et al., “Ethnic differencesin perception of lung function: a factor in pediatric asthmadisparities?” American Journal of Respiratory and Critical CareMedicine, vol. 182, no. 1, pp. 12–18, 2010.

4 Pulmonary Medicine

[15] R. T. Cohen, J. C. Celedon, V. J. Hinckson et al., “Health-careuse among Puerto Rican and African American children withasthma,” Chest, vol. 130, no. 2, pp. 463–471, 2006.

[16] M. P. Foschino Barbaro, D. Lacedonia, G. P. Palladino et al.,“Dyspnea perception in asthma: role of airways inflammation,age and emotional status,” Respiratory Medicine, vol. 105, no. 2,pp. 195–203, 2011.

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