Proceedings of the American Thoracic Society Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mahler, D. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mahler, D. A.
The Proceedings of the American Thoracic Society 3:234-238 (2006)
© 2006 The American Thoracic Society

Mechanisms and Measurement of Dyspnea in Chronic Obstructive Pulmonary Disease

Donald A. Mahler

Dartmouth Medical School, Lebanon, New Hampshire

Correspondence and requests for reprints should be addressed to Donald A. Mahler, M.D., Section of Pulmonary & Critical Care Medicine, Dartmouth-Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH 03756-0001. E-mail: Donald.a.mahler{at}hitchcock.org

ABSTRACT

Patients with chronic obstructive pulmonary disease (COPD) describe their breathlessness as related to the work and effort associated with breathing. Current evidence suggests that the perception of dyspnea is due to a "mismatch" between the outgoing motor command from the central nervous system and the corresponding afferent information from chemoreceptors and/or mechanoreceptors. To measure the severity of dyspnea the principles of psychophysics (stimulus -> response relationship) can be applied. One approach is to consider activities of daily living as a putative stimulus. Although this method relies on patient recall and description of daily tasks, ability to function, as well as time and effort to complete an activity, select clinical instruments have demonstrated appropriate measurement criteria in randomized clinical trials involving patients with COPD. Another approach is for a patient to report the intensity of dyspnea during exercise, and current practice is to provide ratings each minute "on cue" during the exercise test. A computerized system has been developed whereby the person can report ratings spontaneously and continuously by moving a computer mouse that adjusts a vertical bar adjacent to 0–10 category-ratio scale positioned on a monitor. With this continuous method the patient reports twice the number of dyspnea ratings during exercise compared with discrete ratings each minute. Patient-reported dyspnea based on activities of daily living and exercise testing provides distinct but complimentary information.

Key Words: descriptors of breathlessness • clinical dyspnea instruments • exercise testing • neuroventilatory dissociation

Breathing difficulty is the major reason that patients with chronic obstructive pulmonary disease (COPD) seek medical attention. More than 50% of respondents to a telephone survey reported that dyspnea limited sports and recreation activities as well as normal physical exertion (1). About 40% indicated that their breathing affected their ability to perform household chores (1). Unfortunately, many patients with COPD ignore this complaint and mistakenly attribute breathlessness to "getting old" or "being out of shape." Typically, the person decides to be evaluated when dyspnea interferes with work and/or activities of daily living.

MECHANISMS OF DYSPNEA IN COPD

Descriptors of Dyspnea
Dyspnea has been defined as a subjective experience comprised of distinct qualitative sensations which can vary in intensity (2). A variety of studies have demonstrated that patients with different respiratory diseases report unique descriptors of their dyspnea. In particular, those with COPD select statements that relate to the work and/or effort associated with breathing. As an example, the three most common phrases chosen from a list of 15 items by 85 patients with COPD to describe their "uncomfortable awareness of breathing with activities" were (3):

Using cluster analysis, Mahler and coworkers (3) found that the "work/effort" cluster was common in different groups of patients who had various cardiorespiratory disorders. Each diagnosis was associated with a unique set of clusters (e.g., asthma with "work/effort" and "tight"; interstitial lung disease with "work/effort" and "rapid" breathing) (3). In addition, patients with COPD responded that their breathing difficulty was perceived more frequently during inspiration rather than during expiration (3).

In a study by O'Donnell and colleagues (4), the following descriptors of breathlessness were most frequently selected from a list of 16 phrases by patients with COPD immediately after cycle ergometry:

The descriptors of breathlessness chosen by patients with COPD support the concept that inspiratory muscles play an important role in the experience of dyspnea.

Neurophysiologic Model of Dyspnea
Dyspnea may be due to a variety of mechanisms in patients with COPD (Table 1). These different mechanisms may be considered based on a neurophysiological model (5): receptor -> afferent impulse -> integration/processing in the central nervous system (CNS) -> efferent impulse -> dyspnea.


View this table:
[in this window]
[in a new window]
  		TABLE 1. MECHANISMS OF DYSPNEA IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE

 
Receptors.
Ventilatory demand may be increased due to hypoxemia, which stimulates carotid bodies, as well as hypercapnia and/or acidosis, which stimulate the medulla. However, many patients with COPD have an adequate oxygen saturation (>= 90%) and normal or low carbon dioxide levels (<= 40 mm Hg), but still experience dyspnea. In these patients, other mechanisms play a role in their breathing difficulty.

Upper airway and facial mechanoreceptors can modify the perception of breathlessness as evidenced by the observation that some patients prefer to sit by a fan or an open window to allow air movement (6). Dynamic compression of airways during exhalation can stimulate receptors to initiate vagal afferent impulses that contribute to dyspnea in patients with COPD (7). Breathing with pursed lips can modify dyspnea by preventing airway collapse and by providing a sense of control over "the struggle to breathe."

Airway stretch receptors respond to lung inflation. In patients with COPD expiratory airflow limitation can cause hyperinflation at rest and/or during activities that could stimulate stretch receptors. The consequences of hyperinflation include mechanical limitation to increase tidal volume, an increase in the elastic recoil, and shortening of the vertical muscle fibers of the diaphragm (8). The enhanced elastic recoil places an inspiratory "load" on the diaphragm which has functional weakness due to the shorter muscle length resulting from hyperinflation. O'Donnell and coworkers (9) showed that exertional breathlessness ({Delta}Borg at isotime) was significantly correlated (r = 0.50; p = 0.0001) with {Delta} inspiratory capacity at isotime, a measure of dynamic hyperinflation, during constant work exercise on the cycle ergometer in patients with COPD. However, the modest correlation indicates that other factors also contribute to exertional breathlessness.

Both vagal-mediated receptors and nerve fibers located in the airway epithelium and/or alveolar wall respond to a variety of mechanical and chemical stimuli. The improvement in dyspnea reported with inhaled corticosteroids, as well as monoclonal antibody targeting interleukin-8 in patients with COPD, may result from a direct effect of these medications on airway receptors and/or nerve fibers (10–12).

Afferent impulse.
Various nerve pathways can transmit the information after stimulation of the receptor site(s) to the CNS. For example, the vagal nerve transmits afferent information from lung receptors, whereas spinal and supraspinal reflexes are involved in afferent activity from respiratory muscle spindles (2, 5).

Integration/processing in the central nervous system.
Although afferent signals associated with breathlessness are received, integrated, and processed in the CNS, little is actually known about these neural activities. It is believed that motor cortex or brainstem respiratory neurons transmit a signal to the sensory cortex (i.e., corollary discharge), which may contribute to a "sense of effort" to breathe (13). This sensation increases whenever central motor command is increased.

Efferent impulse.
In response to afferent information the CNS sends efferent impulses via the phrenic nerve to the diaphragm and via other motor nerve discharges to the respiratory muscles in order to increase respiration. O'Donnell and colleagues (14) proposed the phrase "neuroventilatory dissociation" to reflect a "mismatch" between afferent information to the CNS and the outgoing motor command to the respiratory muscles. Based on this concept the brain anticipates or expects a certain ventilatory response according to the associated afferent information. Banzett and coworkers (15) termed this process "efferent-reafferent dissociation." This "mismatch theory" of neural activity and subsequent ventilatory outputs appears to contribute to dyspnea under various experimental conditions.

Perception of dyspnea.
Perception of dyspnea is highly variable among individuals with COPD (16–19). For example, patients with COPD exhibit a wide range for magnitude estimation of added resistive loads (17). However, comparison of groups shows that the exponents of the psychophysical power function were similar between patients with COPD and age-matched healthy subjects (17). Noseda and colleagues (16) classified 16 patients with COPD into either "high perceivers" or "low perceivers" based on their ratings of the "change in shortness of breath" after inhalation of saline and after terbutaline. Patients with COPD demonstrate a range of dyspnea responses during exercise testing that are not directly related to the severity of disease (18, 19).

Certainly, psychological factors, such as anxiety, anger, and depression, can increase the severity of breathlessness out of proportion to the physiologic impairment (2). For example, Lavietes and colleagues (20) found that subjects who reported higher ratings of dyspnea while breathing through an inspiratory resistive load had higher depression scores compared with those who had lower ratings of dyspnea. Thus, the psychological profile of patients may contribute to the amplification or exaggeration of the intensity of a symptom such as breathlessness (20). In addition, affective components (i.e., distress associated with breathing difficulty) are common in patients with COPD and can influence any breathing discomfort (21).

MEASUREMENT OF DYSPNEA IN COPD

The two purposes of measuring dyspnea are: to differentiate between patients who have less dyspnea and those who have more dyspnea (discriminate), and to determine whether dyspnea has changed over time and/or as a result of treatment (evaluate). The principles of psychophysics have been applied to develop instruments to quantify the severity of dyspnea (22). Key requirements of the instruments used to measure dyspnea are listed in Table 2.


View this table:
[in this window]
[in a new window]
  		TABLE 2. KEY REQUIREMENTS OF INSTRUMENTS USED TO MEASURE DYSPNEA

 
Clinical Instruments
One approach has been to consider that activities of daily living impact the experience of breathlessness. Over the past 40 years, numerous questionnaires have been developed to quantify the severity of breathlessness based on daily activities (23–36) (Table 3). This approach depends on a patient's recall and description of daily tasks, ability to function, and the time and effort to complete an activity. One of the original questionnaires is the five-point Medical Research Council (MRC) scale developed by Fletcher and coworkers (24). This scale considers a single dimension (i.e., physical tasks such as walking) that provokes breathlessness. The MRC scale has proven to be an excellent discriminative instrument for categorizing patients according to the severity of their breathlessness. In addition, initial scores on the MRC scale have been shown to predict survival in patients with COPD (37, 38). However, the MRC scale is limited as an evaluative instrument because its broad grades make it difficult to detect small but important changes with an intervention (34).


View this table:
[in this window]
[in a new window]
  		TABLE 3. CLINICAL INSTRUMENTS DEVELOPED FOR MEASURING THE SEVERITY OF DYSPNEA

 
Consequently, multidimensional clinical instruments were developed in order to provide a more comprehensive assessment of the severity of dyspnea. The most widely used multidimensional instruments include the Baseline (BDI) and Transition (TDI) Dyspnea Indices (30), which consider three components (functional impairment, magnitude of task, and magnitude of effort), and the dyspnea component of the Chronic Respiratory Disease Questionnaire (CRQ) (31), which incorporates five physical activities that are specific for the individual patient. These instruments have been shown to be valid, reliable, and responsive (39). The responsiveness of the TDI and the dyspnea component of the CRQ have been demonstrated in numerous multicenter randomized clinical trials (i.e., improvements in breathlessness) with pharmacotherapy, pulmonary rehabilitation, and inspiratory muscle training in patients with COPD (9, 11, 40–46).

There has been interest, particularly by regulatory agencies, in determining whether an observed change in a dyspnea score in a randomized clinical trial is meaningful to the patient group. The concept of minimal clinically important difference (MCID) has developed to examine the smallest improvement in an outcome that is considered meaningful to the individual patient. Based on different methods (expert preference; anchor approach; and distribution estimates), the MCID has been determined to be one unit for the TDI (47, 48) and 0.5 unit for the dyspnea component of the CRQ (49).

An important characteristic for measuring dyspnea is that the score or grade be patient reported. Both the original BDI/TDI and the dyspnea component of the CRQ were developed so that a physician, nurse, or technician could interview an individual patient in order to inquire about how various aspects of the person's life might affect his/her breathlessness. According to the patient's answers, the interviewer would then select (for the BDI/TDI), or help the patient select (for the CRQ), a grade for breathlessness for each dimension or activity. Recently, both instruments have been developed into self-administered versions so that the dyspnea grades represent direct patient-reported measures rather than be influenced by possible bias or interpretation by the interviewer (33–36). These self-administered instruments represent a standardized approach for obtaining a patient's report of the severity of breathlessness based on specific questions or activities.

Exercise Testing
Another approach for measuring dyspnea is for the patient to rate the intensity of dyspnea on a scale while exercising on a cycle ergometer or on a treadmill (18, 50). This method attempts to simulate the person's experience while performing physical activities. Although the precise stimulus for exertional breathlessness is not completely understood, for measurement purposes it is reasonable to consider power production (watts) and/or oxygen consumption (ml/kg/min) as putative "stimuli" for provoking dyspnea during exertion (18, 50). Typically, subjects provide ratings of dyspnea during exercise on the 0–10 category-ratio scale (CR-10) developed by Borg (51) or on a visual analog scale (VAS) (52). The CR-10 scale has two major advantages for measuring dyspnea during exercise testing. The presence of descriptors on the CR-10 scale permits comparisons between individuals based on the assumption that the verbal descriptors on the scale have similar meaning to different subjects (51). In addition, a value on the CR-10 scale may be used as a dyspnea "target" for patients to monitor the intensity of their exercise training (53).

Initial investigations had subjects rate dyspnea at the end of the exercise test (i.e., peak values). In general, both healthy individuals and patients with cardiorespiratory disease reported peak ratings between 5 and 8 on the CR-10 scale (54). These findings led to the standard practice of instructing patients to give ratings at each minute "on cue" during the exercise test (18, 50). By combining the physiologic variables (e.g., power production or oxygen consumption) with these discrete dyspnea ratings, it is possible to calculate a slope and an intercept of the stimulus -> response relationship (18, 19, 50). In general, the slope of the regression between power production and dyspnea ratings is higher in patients with respiratory disease compared with healthy individuals (18, 19).

The majority of exercise studies involving patients with COPD have used the cycle ergometer for diagnostic testing to evaluate breathlessness and for assessing response to therapy. The rationale for using the cycle ergometer is that the work load can be quantified and older patients may feel safer during exertion because their weight is supported. However, the majority of patients are more familiar with walking rather than cycling. Man and coworkers (55) showed that patients with COPD selected higher ratings for dyspnea while walking, but generally reported higher ratings for leg discomfort while cycling. Additional testing will be required to examine which mode of exercise is preferable to evaluate the patient's experience of dyspnea.

In 1993 Harty and colleagues (56) described the methodology and results of the continuous measurement of breathlessness during exercise in six healthy subjects who used a potentiometer to give their ratings on a VAS displayed on a monitor. In 2001 Mahler and coworkers (57) reported on a continuous method in which subjects moved a computer mouse that controlled the length of a bar (i.e., a VAS) whose lower edge coincided with a value along the CR-10 scale to represent the current level of perceived dyspnea throughout exercise. This approach allows the subject to provide ratings spontaneously and continuously while exercising without waiting for a cue or request from the physician. In general, subjects report about twice the number of dyspnea ratings during exercise while using the continuous method compared with the discrete method (i.e., ratings each minute) (19, 57).

There are three important advantages of the continuous method for measuring dyspnea. First, the perception of breathlessness may change throughout the course of exercise rather than at arbitrary one-minute time intervals. Thus, the standard approach obtaining discrete ratings each minute may not accurately reflect the perceptual changes in dyspnea. Second, the continuous method enables subjects to provide, on average, about twice the number of dyspnea ratings compared with the discrete method. This may be important because some patients with respiratory disease may only be able to exercise for three or four minutes; consequently, only a few dyspnea ratings may be obtained with the discrete method (19, 57). Certainly, statistical analyses may be difficult when trying to fit a quantitative function to only a few data points. Third, this system incorporates a VAS positioned adjacent to the CR-10 scale that provides a continuous measure for patients to rate breathlessness, whereas the discrete method provides only integer choices on the CR-10 scale.

The validity of the continuous system for subjects to report the intensity of dyspnea during exercise has been established in healthy young and old adults as well as in patients with COPD (19, 57). In addition, this methodology has demonstrated responsiveness to acute interventions such as breathing through an inspiratory resistive load (57) and administration of short-acting bronchodilator therapy (58).

CONCLUSIONS
Various pathophysiologic mechanisms can contribute to dyspnea in patients with COPD. Current understanding suggests that a "mismatch" between neural activity from the brain and consequent ventilatory output from the respiratory muscles contributes to the perception of breathlessness. To quantify the intensity of dyspnea, various questionnaires/scales have been developed that have demonstrated validity, reliability, and responsiveness. Recently, two widely used clinical instruments, the BDI/TDI and the dyspnea component of the CRQ, have been modified into self-administered versions so that the patient can report directly the impact of activities of daily living on dyspnea. These questionnaires are appropriate for randomized clinical trials involving large numbers of subjects, as dyspnea scores can be obtained easily with minimal equipment and cost. Another approach uses exercise testing whereby the patient reports discrete (e.g., each minute) or continuous (e.g., whenever there is a change) ratings of dyspnea while exercising. Both the discrete and continuous methods can be used during cardiopulmonary exercise testing for clinical and research purposes.

FOOTNOTES

Conflict of Interest Statement: D.A.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript.

(Received in original form September 21, 2005; accepted in final form December 16, 2005)

REFERENCES

  1. Rennard S, Decramer M, Calverly PMA, Pride NB, Soriano JB, Vermeire PA, Vestbo J. Impact of COPD in North America and Europe in 2000: subjects' perspective of confronting COPD. International Survey. Eur Respir J 2002;20:799–805.[Abstract/Free Full Text]
  2. American Thoracic Society. Dyspnea: mechanisms, assessment, and management: a consensus statement. Am J Respir Crit Care Med 1999;159:321–340.[Free Full Text]
  3. Mahler DA, Harver A, Lentine T, Scott JA, Beck K, Schwartzstein RM. Descriptors of breathlessness in cardiorespiratory diseases. Am J Respir Crit Care Med 1996;154:1357–1363.[Abstract]
  4. O'Donnell DE, Bertley JC, Chau LK, Webb KA. Qualitative aspects of exertional breathlessness in chronic airflow limitation: pathophysiologic mechanisms. Am J Respir Crit Care Med 1997;155:109–115.[Abstract]
  5. Manning HL, Schwartzstein RM. Pathophysiology of dyspnea. N Engl J Med 1995;333:1547–1553.[Free Full Text]
  6. Schwartzstein RM, Lahive K, Pope A, Weinberger SE, Weiss JW. Cold facial stimulation reduces breathlessness induced in normal subjects. Am Rev Respir Dis 1987;136:58–61.[Medline]
  7. O'Donnell DE, Sanii R, Anthonisen NR, Younes M. Effect of dynamic airway compression on breathing pattern and respiratory sensation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis 1987;135:912–918.[Medline]
  8. O'Donnell DE, Webb KA. Exertional breathlessness in patietns with chronic airflow limitation: the role of lung hyperinflation. Am Rev Respir Dis 1993;148:1351–1357.[Medline]
  9. O'Donnell DE, Fluge T, Gerken F, Hamilton A, Webb K, Aguilaniu B, Make B, Magnussen H. Effects of tiotropium on lung hyperinflation, dyspnoea and exercise tolerance in COPD. Eur Respir J 2004;23:832–840.[Abstract/Free Full Text]
  10. Calverly P, Pauwels R, Vestbo J, Jones P, Pride N, Gulsvik A, Anderson J, Maden C. Combined salmeterol and fluticasone in the treatment of chronic obstructive pulmonary disease: a randomised controlled trial. Lancet 2003;361:449–456.[CrossRef][Medline]
  11. Mahler DA, Wire P, Horstman D, Chang CN, Yates J, Fischer T, Shah T. Effectiveness of fluticasone propionate and salmeterol combination delivered via the diskus device in the treatment of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2002;166:1084–1091.[Abstract/Free Full Text]
  12. Mahler DA, Huang S, Tabrizi M, Bell GM. Efficacy and safety of a monoclonal antibody recognizing interleukin-8 in COPD: a pilot study. Chest 2004;126:926–934.[Abstract/Free Full Text]
  13. Killian KJ, Gandevia SC, Summer E, Campbell EJM. Effect of increased lung volume on perception of breathlessness. J Appl Physiol 1984;57:686–691.[Abstract/Free Full Text]
  14. O'Donnell DE, Webb KA. Exertional breathlessness in patients with chronic airflow limitation. Am Rev Respir Dis 1993;148:1351–1357.[Medline]
  15. Banzett RB, Lansing RW, Brown R. "Air hunger" from increased PCO2 persists after complete neuromuscular block in humans. Respir Physiol 1990;81:1–17.[CrossRef][Medline]
  16. Noseda A, Schmerber J, Prigogine T, Yernault JC. Perceived effect on shortness of breath of an acute inhalation of saline or terbutaline: variability and sensitivity of a visual analogue scale in patients with asthma or COPD. Eur Respir J 1992;5:1043–1053.[Abstract]
  17. Mahler DA, Rosiello RA, Harver A, Lentine T, McGovern JF, Daubenspeck JA. Comparison of clinical dyspnea ratings and psychophysical measurements of respiratory sensation in obstructive airway disease. Am Rev Respir Dis 1987;135:1229–1233.[Medline]
  18. Hamilton AL, Killian KJ, Summers E, Jones NL. Symptom intensity and subjective limitation to exercise in patients with cardiorespiratory disorders. Chest 1996;110:1255–1263.[Abstract/Free Full Text]
  19. Fierro-Carrion G, Mahler DA, Ward J, Baird JC. Comparison of continuous and discrete measurements of dyspnea during exercise in patients with COPD and normal subjects. Chest 2004;125:77–84.[Abstract/Free Full Text]
  20. Lavietes MH, Sanchez CW, Tiersky LA, Cherniack NS, Natelson BH. Psychological profile and ventilatory response to inspiratory resistive loading. Am J Respir Crit Care Med 2000;161:737–744.[Abstract/Free Full Text]
  21. Carrieri-Kohlman V, Gormley JM, Douglas MK, Paul SM, Stulbarg MS. Differentiation between dyspnea and its affective components. West J Nurs Res 1996;18:626–642.[Abstract/Free Full Text]
  22. Baird JC, Noma E. Fundamentals of scaling and psychophysics. New York: Wiley Interscience; 1978.
  23. Fletcher CM. The clinical diagnosis of pulmonary emphysema - an experimental study. Proc R Soc Med 1952;45:577–584.[Medline]
  24. Fletcher CM, Elmes PC, Wood CH. The significance of respiratory symptoms and the diagnosis of chronic bronchitis in a working population. BMJ 1959;2:257–266.[Free Full Text]
  25. Aitken RCB. Measurement of feelings using visual analogue scales. Proc R Soc Med 1969;62:989–993.[Medline]
  26. McGavin CR, Artvinli M, Naoe H. Dyspnea, disability, and distance walked: comparison of estimates of exercise performance in respiratory disease. BMJ 1978;2:241–243.[Abstract/Free Full Text]
  27. Rose GA, Blackburn H, Gillum RF. Cardiovascular survey methods, 2nd ed. Geneva: World Health Organization; 1982. p. 166. WHO Monograph Series, No. 56, Annex 7.
  28. Brooks SM. Task force on surveillance for respiratory hazards in the occupational setting. Surveillance for respiratory hazards. ATS News 1982;8:12–16.
  29. Leidy NK, Rennard SI, Schmier J, Jones KC, Goldman M. The breathlessness, cough, and sputum scale. Chest 2003;124:2182–2191.[Abstract/Free Full Text]
  30. Mahler DA, Weinberg DH, Wells CK, Feinstein AR. The measurement of dyspnea: contents, interobserver agreement, and physiologic correlates of two new clinical indexes. Chest 1984;85:751–758.[Abstract/Free Full Text]
  31. Guyatt GH, Berman LB, Townsend M, Pugsley SO, Chambers LW. A measure of quality of life for clinical trials in chronic lung disease. Thorax 1987;42:773–778.[Abstract/Free Full Text]
  32. Eakin EG, Resnikoff PM, Prewitt LM, Ries AL, Kaplan RM. Validation of a new dyspnea measure: the UCSD shortness of breath questionnaire. Chest 1998;113:619–624.[Abstract/Free Full Text]
  33. Mahler DA, Ward J, Fierro-Carrion G, Waterman LA, Lentine TF, Mejia-Alfaro R, Baird JC. Development of self-administered versions of modified Baseline and Transition Dyspnea Indexes in COPD. J COPD 2004;1:165–172.
  34. Mahler DA, Waterman LA, Ward J, Lentine TF, Tomlinson D, Baird JC. Validity and responsiveness of the self-administered computerized (SAC) versions of the Baseline (BDI) and Transition (TDI) Dyspnea Indexes in COPD [abstract]. Proc Am Thoracic Soc 2005;2:A643.
  35. Williams JE, Singh SJ, Sewell L, Morgan MD. Health status measurement: sensitivity of the self-reported chronic respiratory questioinnaire (CRQ-SR) in pulmonary rehabilitation. Thorax 2003;58:515–518.[Abstract/Free Full Text]
  36. Schunemann HJ, Goldstein R, Mador MJ, McKim D, Stahl E, Puhan M, Griffith LE, Grant B, Austin P, Collins R, et al. A randomised trial to evaluate the self-administered standardised chronic respiratory questionnaire. Eur Respir J 2005;25:31–40.[Abstract/Free Full Text]
  37. Nishimura K, Izumi T, Tsukino M, Oga T. Dyspnea is a better predictor of 5-year survival than airway obstruction in patients with COPD. Chest 2002;121:1434–1440.[Abstract/Free Full Text]
  38. Celli BR, Cote CG, Marin JM, Casanova C, Montes de Oca M, Mendez RA, Pinto Plata V, Cabral HJ. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med 2004;350:1005–1012.[Abstract/Free Full Text]
  39. Mahler DA. Measurement of dyspnea: clinical ratings. In: Mahler DA, O'Donnell DE, eds. Dyspnea: mechanisms, measurement, and management. New York: Taylor & Francis Books, Inc.; 2005. pp. 147–164.
  40. O'Donnell DE, McGuire MA, Samis L, Webb KA. The impact of exercise reconditioning on breathlessness in severe chronic airflow limitation. Am J Respir Crit Care Med 1995;152:2005–2013.[Abstract]
  41. Vincken W, van Noord JA, Greefhorst APM, Bantje TA, Kesten S, Korducki L, Cornelissen PJG. Improved health outcomes in patients with COPD during 1 yr's treatment with tiotropium. Eur Respir J 2002;19:209–216.[Abstract/Free Full Text]
  42. Casaburi R, Mahler DA, Jones PW, Wanner A, San Pedro G, ZuWallack RL, Menjoge SS, Serby CW, Witek T Jr. A long-term evaluation of once-daily inhaled tiotropium in chronic obstructive pulmonary disease. Eur Respir J 2002;19:217–224.[Abstract/Free Full Text]
  43. Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabiliatation on physiologic and psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995;122:823–832.[Abstract/Free Full Text]
  44. Readon J, Awad E, Normandin E, Vale F, Clark B, ZuWallack RL. The effect of comprehensive outpatient pulmonary rehabilitation on dyspnea. Chest 1994;105:1046–1052.[Abstract/Free Full Text]
  45. Martinez FJ, Montes de Oca M, Whyte RI, Stetz J, Gay SE, Celli BR. Lung-volume reduction improves dyspnea, dynamic hyperinflation, and respiratory muscle function. Am J Respir Crit Care Med 1997;155:1984–1990.[Abstract]
  46. Lisboa C, Munoz V, Beroiza T, Leiva A, Cruz E. Inspiratory muscle training in chronic airflow limitation: comparison of two different training loads with a threshold device. Eur Respir J 1994;7:1266–1274.[Abstract]
  47. Witek TJ Jr, Mahler DA. Meaningful effect size and patterns of response of the transiiton dyspnea index. J Clin Epidemiol 2003;56:248–255.[CrossRef][Medline]
  48. Witek TJ Jr, Mahler DA. Minimal important difference of the transition dyspnoea index in a multinational clinical trial. Eur Respir J 2003;21:1–6.[Free Full Text]
  49. Schunemann HJ, Puhan M, Goldstein R, Jaeschke R, Guyatt GH. Measurement properties and interpretability of the Chronic Respiratory Disease Questionnaire. J COPD 2005;2:81–89.[Medline]
  50. Mahler DA, Fierro-Carrion G, Baird JC. Mechanisms and measurement of exertional dyspnea. In: Weisman IM, Zeballos RJ, editors. Clinical exercise testing. Progress in Respiratory Research, vol. 32. Basel: Karger; 2002;32:72–80.
  51. Borg GAV. Psychological bases of perceived exertion. Med Sci Sports Exerc 1982;14:377–381.[Medline]
  52. Gift AG. Visual analogue scales: measurement of subjective phenomena. Nurs Res 1989;38:286–288.[Medline]
  53. Mejia R, Ward J, Lentine T, Mahler DA. Target dyspnea ratings predict expected oxygen consumption as well as target heart rate values. Am J Respir Crit Care Med 1999;159:1485–1489.[Abstract/Free Full Text]
  54. Killian KJ, LeBlanc P, Martin DH, Summers E, Jones NL, Campbell EJM. Exercise capacity and ventilatory, circulatory, and symptom limitation in patients with chronic airflow limitation. Am Rev Respir Dis 1992;146:935–940.[Medline]
  55. Man WD, Soliman MG, Gearing J, Radford SG, Rafferty GF, Gray BJ, Polkey MI, Moxham J. Symptoms and quadriceps fatigability after walking and cycling in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2003;168:562–567.[Abstract/Free Full Text]
  56. Harty HR, Heywood P, Adams L. Comparison between continuous and discrete measurements of breathlessness during exercise in normal subjects using a visual anlogue scale. Clin Sci 1993;85:229–236.[Medline]
  57. Mahler DA, Mejia-Alfaro R, Ward J, Baird JC. Continuous measurement of breathlessness during exercise: validity, reliability, and responsiveness. J Appl Physiol 2001;90:2188–2196.[Abstract/Free Full Text]
  58. Mahler DA, Fierro-Carrion G, Mejia-Alfaro R, Ward J, Baird JC. Responsiveness of continuous ratings of dyspnea during exercise in patients with COPD. Med Sci Sports Exerc 2005;37:529–535.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 ERRHome page
C. J. Jolley and J. Moxham
A physiological model of patient-reported breathlessness during daily activities in COPD
Eur. Respir. Rev., June 1, 2009; 18(112): 66 - 79.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
A. von Leupoldt, S. Balewski, S. Petersen, K. Taube, S. Schubert-Heukeshoven, H. Magnussen, and B. Dahme
Verbal Descriptors of Dyspnea in Patients With COPD at Different Intensity Levels of Dyspnea
Chest, July 1, 2007; 132(1): 141 - 147.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mahler, D. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mahler, D. A.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS