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A MANUAL FOR PULMONARY REHABILITATION IN AUSTRALIA

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A MANUAL FOR PULMONARY
REHABILITATION IN AUSTRALIA
EVIDENCE BASE AND STANDARDS
Peter Frith
Professor and Head of Southern Respiratory Services
Flinders University and Southern Adelaide Health Service
(Repatriation General Hospital and Flinders Medical Centre)
South Australia
1
TABLE OF CONTENTS
A MANUAL FOR PULMONARY REHABILITATION IN AUSTRALIA
1
EVIDENCE BASE AND STANDARDS
1
Executive Summary
Description of Pulmonary Rehabilitation (PR)
5
5
Evidence Statements
5
Evidence-Based Recommendations
8
1.
INTRODUCTION
History and Role of the Australian Lung Foundation in Research and Patient Care
Program of Evidence-Based Supports for Pulmonary Rehabilitation in Australia
2.
DEFINITIONS AND DESCRIPTIONS
2.1
Chronic Obstructive Pulmonary Disease (COPD)
11
11
12
15
15
2.2
Clinical Indicators and Outcome Measures
Health outcomes
Health Economic Outcomes
Indicators of Respiratory Impairment
Indicators of Psychological Impairment
Indicators of Nutritional Impairment
Activities of Daily Living
Quality of Life
19
19
20
21
24
24
25
26
2.3
Disease Management
29
2.4
Impairment, Disability and Handicap
31
2.5
Outreach and Home Care
32
2.6
Pulmonary Rehabilitation (PR)
32
2.7
Self-Management for Chronic Disease
33
2.8
Support Groups
34
3.
EPIDEMIOLOGY AND BURDEN OF CHRONIC LUNG DISEASE
3.1
Prevalence and Incidence
3.2
Risk factors for COPD
Age
Gender
Race/Ethnicity
Asthma and Airway Hyper-responsiveness
36
36
40
42
43
43
44
Smoking
Biomass Smoke
Occupational Exposure
Environment (Air Pollution)
Socioeconomic Status
Nutrition
Lung Growth
45
46
46
47
48
48
49
3.3
Mortality
50
3.4
Morbidity and Burden of Illness
52
3.5
Costs
53
3.6
Carer Burden
55
3.7
Assessing COPD Severity
58
3.8
Exacerbations of COPD
59
3.9
Management of COPD
62
4.
PULMONARY REHABILITATION
4.1
Introduction
Rehabilitation within Lung Disease Management
Management of COPD
Goals of Pulmonary Rehabilitation
Benefits of Pulmonary Rehabilitation
Components of Pulmonary Rehabilitation
71
71
71
71
79
80
81
4.2
Overviews of COPD and Rehabilitation
Evidence review 1971-1994
Evidence reviews 1995-2001, 2001-2004, 2006 and 2008
Peripheral muscle impairments
Physical Training
Education
Physiotherapy
Psychological Interventions
Nutritional Interventions
Comprehensive Pulmonary Rehabilitation
81
81
84
86
89
109
118
123
130
132
4.3
Health Economics and Pulmonary Rehabilitation
136
4.4
Shared care and self-management
137
4.5
Support Groups for Patients and Carers
144
4.6
Staffing for Pulmonary Rehabilitation
Staffing Philosophies
Structure
Communication
5.
CLINICAL INDICATORS AND OUTCOME MEASUREMENT
146
147
147
149
151
3
5.1
Respiratory Symptoms
Dyspnoea
151
151
5.2
Measures of Impairment
Physiological Impairments
Tests of Static Physiological Impairment
Key Points
Exercise impairment
Nutritional Impairments
Psychological Impairments
157
157
161
161
161
168
171
5.3
Indicators of Functional Disability and Handicap
Functional Exercise Endurance
Functional Disability Questionnaires
175
175
176
APPENDIX 1
194
Pulmonary rehabilitation programs in Australia
194
A.1.1.
ALF Better Breathing Program Survey of Patient Perspectives of Pulmonary Rehabilitation 194
A.1.2.
ALF Better Breathing Program Survey of Pulmonary Rehabilitation Programs in Australia 197
A.1.3.
ALF Patients Needs Analysis
199
A,1.4.
Pulmonary Rehabilitation Survey, 2007
200
A.1.5.
Comprehensive Pulmonary Rehabilitation.
202
A Sample Program
202
APPENDIX 3
Submissions to ALF
205
205
4
Executive Summary
This “Manual for Pulmonary Rehabilitation In Australia: Evidence Base and Standards” provides a
comprehensive review of evidence relevant to pulmonary rehabilitation as a support for pulmonary
rehabilitation practice and management in Australia. A Pulmonary Rehabilitation Toolkit has been
developed to assist new practitioners and administrators, and to enable continuous quality improvement for
established programs. The Australian Lung Foundation (ALF) with the Thoracic Society of Australia and
New Zealand (TSANZ) and Australian Physiotherapy Association (APA) helped in the development and
implementation of the suite of tools supporting management of chronic obstructive pulmonary disease
(COPD), which currently includes evidence-based practice guidelines for COPD (known as �COPD-X’), a
diagnostic algorithm, a COPD-Checklist, COPD Action Plans, the Pulmonary Rehabilitation Toolkit, and
this Manualв€—
Description of Pulmonary Rehabilitation (PR)
Pulmonary rehabilitation (PR) is a system of care that includes education, exercise training and
psychosocial support delivered by an interdisciplinary team of therapists. It was originally
designed for people with moderate to severe COPD, but those with other respiratory disorders
who have disabling breathlessness can also benefit. Although it does not alter traditional lung
function parameters [Level II], PR can help people achieve and maintain a maximum level of
independence and functioning in the community [Level I]. It has favourable interactions with
other interventions [Level II], particularly nutritional and pharmacotherapeutic, and can be
delivered in a range of settings. Single modality treatments also have benefit.
Evidence Statements
Comprehensive Integrated Rehabilitation
Each component of PR is beneficial, but comprehensive integrated programs have greater
efficacy. Effective PR requires close liaison among care providers and a philosophy of support
for informal caregivers as well as the patient. Patient-specific goal-setting within a biopsychosocial paradigm, communicated to all care providers, should be reviewed regularly. As
benefits wane after six to twelve months, continuing exercise should be encouraged, knowledge
should be updated regularly, and social support structures should be optimised.
Meta-analyses and randomised controlled trials show that comprehensive Pulmonary
Rehabilitation enhances health-related quality of life and self-efficacy, improves exercise
performance and mental health, reduces breathlessness, and reduces health care utilisation (and
associated costs) more effectively than each component. [Level I]
Exercise training
Exercise training includes aerobic training of upper and lower limbs and trunk muscles, flexibility
and muscle strength, guiding efficient energy expenditure, and teaching breathing control during
в€—
http://www.copdx.org.au/ and http://www.pulmonaryrehab.com.au, or
http://www.lungnet.com.au/copd/PR_Toolkit.html
exertion. Supervision helps build patient confidence, maximises skeletal muscle training, teaches
breathing techniques, optimises cardiovascular fitness, and encourages exercise maintenance.
Large randomised controlled trials and meta-analyses of exercise training alone in COPD have
shown improvements in cardiovascular fitness, exercise tolerance, breathlessness, muscle
strength, functioning, self-efficacy, mood and health-related quality of life. Training of multiple
muscle groups is more beneficial than confining exercise to upper or lower limbs or to
inspiratory muscles alone. [Level I]
Education
Education improves the patient’s knowledge about breathing and the various treatments to control
breathlessness. Of primary importance is assisting smokers to quit and sustain quitting. Patients
should be trained to optimise activities and nutrition, gain control over anxiety, panic or
depression, and use appropriate medications and therapeutic devices effectively. A background of
respiratory anatomy and physiology is traditionally given, to assist with problem solving and
building the patient's capacity to co-manage their condition.
Small randomised trials of education alone show better self-efficacy, mood and health-related
quality of life, above usual medical care, though the evidence for education alone is less robust
than for exercise. [Level II]
Psychosocial support
Depression, anxiety and panic are frequent complications of chronic disabling breathlessness,
with dependency and social isolation being common consequences. General support, specific
behavioural training and use of appropriate antidepressant medications where needed may
enhance quality of life for the patient and the family caregiver.
Small randomised controlled trials show better exercise tolerance, mood, self-efficacy and
health-related quality of life from cognitive behaviour therapy alone in COPD. There is limited
evidence that anxiolytics or antidepressant medications can help some people. [Level II]
6
Roles and Responsibilities of Health Professionals
Health professionals involved in PR should have a high level of understanding about COPD and
other chronic respiratory diseases, and the relevance of disability and handicap. They and their
employers should recognise and respect the roles of all members of the care partnership,
including the patent and family caregivers. They should have commitment to quality of care and
continuous improvement. They should understand clinical indicators that reflect risk factors, and
outcome measurements that reflect changes in impairment, disability and cost-effectiveness. They
need to be timely, clear and relevant when communication with each patient’s health care
providers. Above all, they must remember that PR represents an ideal opportunity to alter
people’s lives for the better and that it should contribute to their patients’ lifetime care. [Level IV]
Patient Goals
Patients should be encouraged to explore their own needs and to plan their goals of treatment
accordingly. After completing PR patients should be confident to monitor and manage their lung
condition more effectively so they will have fewer sudden exacerbations and need for emergency
treatment, and their dependency level is reduced. PR should enable patients to collaborate in an
informed manner with their doctor and other care providers in planning their own care. [Level III3] Their informal caregivers should also feel more confident and less restricted. [Level IV]
Levels of Evidence
Throughout all ALF documents a similar system for recording levels of evidence is used.
Level
I
II
III-1
III-2
III-3
IV
Sources of Evidence
systematic review of all relevant randomised controlled trials
at least one properly designed randomised controlled trial
well-designed controlled studies without randomization
well-designed cohort or case-control studies preferably from more than one centre or group
multiple time series, including dramatic results in uncontrolled experiments
opinions of respected authorities, case series, descriptive studies, or reports of expert committees
Strength of Recommendations
The strength of support for recommended management is graded in a standard way throughout all ALF documents.
Grade
Description
Rich body of data
Sources
Randomised
controlled trials
B
Limited body of
data
Randomised
controlled trials
C
Very limited data
D
Opinion
Non-randomised
trials.
Observational
studies.
Panel consensus.
Judgement.
A
Definition
Evidence from well-designed RCTs with clear endpoints providing
consistent patterns of outcomes, involving large numbers of studies
with substantial numbers of participants systematically reviewed in
meta-analysis. This implies very low risk of bias, high degree of
consistency, and direct applicability to the target population.
Evidence from intervention studies that include limited numbers of
participants, sub-group analysis of RCTs, case control or cohort
studies. This implies good quality evidence with low risk of
confounding or bias, and good applicability to the target population.
Evidence from outcomes of uncontrolled or non-randomised trials or
from observational studies, well conducted case control or cohort
studies with low risk of confounding and moderate applicability to
the target population.
Little direct evidence apart from case studies, case reports, or
opinions of respected authorities, extrapolated from clinical
experience, cohort studies with potential confounding bias,
descriptive studies or reports of expert committees.
7
Evidence-Based Recommendations
1.
Comprehensive pulmonary rehabilitation should be an integral part of treatment
for all people with moderate to severe COPD (A), as it provides extra benefits over standard
medical care in terms of clinically and statistically significant improvements in:
Exercise capacity (A)
Health-related quality of life (A)
Psychosocial problems (B)
Dyspnoea (A)
Fatigue (A)
Functional status (A)
Mastery and self-efficacy (A)
2.
Comprehensive pulmonary rehabilitation should be considered for people with
other disabling lung conditions. The following in particular are recommended:
Training for correct use of and asthma medications and devices (A)
Training for ensuring adherence to asthma treatment plan (A)
Exercise conditioning for people with asthma (B)
Sputum clearance for people with bronchiectasis including Cystic Fibrosis (B)
Education, psychosocial support, relaxation and exercise training for people with Pulmonary
Fibrosis (D)
3.
Exercise training for people with COPD is more effective than standard medical
care, in terms of:
Exercise capacity (B)
Health-related quality of life (B)
Fatigue (B)
4.
Additional benefit from exercise training may be provided by
Breathing control (slower deeper breathing pattern) (B)
Oxygen supplementation – inconsistent evidence (B)
Helium-oxygen breathing (B)
Use of long-acting bronchodilator (tiotropium) (B)
5.
Educational training alone for people with COPD appears more effective than
standard medical care, in terms of:
Health-related quality of life (B)
Self-efficacy (B)
Mastery (B)
Dyspnoea (C)
Functional status (C)
Psychosocial problems (C)
6.
Psychosocial support through pulmonary rehabilitation and/or support groups is
recommended for people with disabling COPD, as it is effective for the patient in terms of:
Self-efficacy (B)
Mastery (C)
Depression (C)
Panic disorder (D)
8
Functional status (B)
Health-related quality of life (B)
Carer health (D)
7.
Pulmonary rehabilitation is effective in a variety of settings, including hospital
inpatients (A), hospital outpatients (A) and community settings (B).
8.
Core staff for pulmonary rehabilitation should be health professionals who understand
lung and exercise physiology, pharmacology, and psychosocial issues (D).
9.
The Program Director should be a health professional with a high level of commitment
to outcome evaluation, quality improvement and economic aspects (D). The appointment will
depend on local requirements and staff limitations.
10.
A medical consultant should take a lead role in program content, patient assessment
and program safety supervision (D). Medical input into educational training is also recommended
(D).
11.
A referral process should be agreed with consumers, administrators and
professionals, and adhered to (D), taking into account local needs and limitations. Referring
professionals should be required to document all conditions and treatments applicable to the
patient.
12.
All patients referred for pulmonary rehabilitation should undergo an initial clinical
assessment (D), to include as a minimum:
Age, gender, racial or ethnic background, occupations, family respiratory history
Place of residence and presence of family caregiver, plus other important supports
Smoking status (past and present, quantity, readiness to quit if still smoking, level of nicotine
dependence and other habit issues)
Nutritional status (current weight and body mass index, recent weight loss)
Functional status (mobility, causes of limitations)
Primary respiratory and secondary diagnoses (comorbidities & complications of the primary
disease or treatment)
Pharmaceutical and other treatments (oxygen, physical, psychological, and complementary)
Patient perceived problems and their goals
13.
All patients enrolled in pulmonary rehabilitation should have documentation of
clinical indicators (D), which should address
Nutritional measures (eg height, weight, body mass index, etc)
Symptoms and dyspnoea scoring (eg MRC Dyspnoea Grade, etc)
Respiratory impairment (eg spirometry, gas transfer, etc)
Mental health status (eg General Health Questionnaire, Hospital Anxiety and Depression
Scale, etc)
Level of disability (eg 6-minute walk, shuttle walk, functional index, etc)
Level of handicap (eg functional / ADL assessment)
Health-related quality of life (eg St George Respiratory Questionnaire, SF-36, etc)
Current level of achievement of negotiated goals
14.
All patients completing pulmonary rehabilitation should have changes in outcome
measures documented, addressing the above clinical indicators (D)
9
15.
Timely feedback should be provided to health professionals involved in the care of
each patient (whether referring the patient or not) (D) about:
Initial assessments and recommendations relating to new findings
Post-program assessments and recommendations for ongoing care
Long-term assessments
10
1. INTRODUCTION
This Manual aims to provide comprehensive information for health workers and other providers,
administrative boards, governments, insurers and other interested bodies relating to Pulmonary
Rehabilitation and its application in Australia. Recommendations are based on current scientific evidence,
guidelines from the USA1,2, UK3 and Europe4, systematic reviews, meta-analyses and careful literature
review. American and European specialist societies have joined forces in a joint Statement more recently5,
and the AACP/AACVPR Clinical Practice Guidelines have also been updated6. Data from ALF surveys of
patients and professionals provide nationally relevant information about program availability, patient
perceptions and an understanding of what constraints exist to providing or accessing this form of therapy in
Australia.
The Manual should assist professionals and organisations wishing to develop programs that are relevant to
the needs and demographics of the local community. It forms the evidence base for the Pulmonary
Rehabilitation Toolkit, which provides direct assistance, through http://www.pulmonaryrehab.com.au, or
http://www.lungnet.com.au/copd/PR_Toolkit.html
References are placed for immediate ease of access as footnotes on the same page. This should reduce the
need for cross-referencing, and each section can be read independently. Key Points are emphasized
throughout in shaded Boxes as helpful summaries. Submissions and special reports that form the basis for
Australian application are available as a set of Appendices but are not published in this main document.
History and Role of the Australian Lung
Foundation in Research and Patient Care
The Australian Lung Foundation (ALF) has had a charter since the late 1980's to improve the wellbeing of
people with respiratory conditions and to promote lung health in Australia. It seeks to achieve these by:
o Raising funds in support of medical research into lung diseases
o Distributing research findings and knowledge
o Educating patients and the broader public on the prevention, early detection and effective treatment of
lung diseases
o Fostering patient support activities
o Influencing public and corporate policy to ensure safe living and working environments and equitable
access to quality health care
In 1995 the ALF convened a National Lung Research Summit to determine priorities, from which came the
recommendation for the formation of multi-disciplinary condition-related Consultative Groups – aiming to
develop priorities in respiratory health, and supporting holistic patient care and research. The Chronic
Airflow Limitation Consultative Group was established in 1997 and later became the COPD Coordinating
1
AACVPR/ACCP Pulmonary Rehabilitation Guidelines Panel. Pulmonary Rehabilitation. Joint
ACCP/AACVPR evidence-based guidelines. Chest 1997; 112:1363-1396
2
American Association of Cardiovascular and Pulmonary Rehabilitation. Guidelines for Pulmonary
Rehabilitation Programs 2nd edition. Champaign IL: Human Kinetics 1998
3
British Thoracic Society Standards of Care Subcommittee on Pulmonary Rehabilitation. Pulmonary
rehabilitation. Thorax 2001; 56:827-834
4
Donner CF, Muir JF. Selection criteria and programmes for pulmonary rehabilitation in COPD patients.
Eur Respir J 1997; 10:744-757
5
Nici L, Donner C, Wouters E, Zuwallack R, et al. American Thoracic Society/European Respiratory
Society Statement on Pulmonary Rehabilitation. Am J Respir Crit Care Med 2006; 173:1390-1413
6
Ries AL, Bauldhoff GS, Carlin BW, Casaburi R, et al. Pulmonary Rehabilitation: Joint ACCP/AACVPR
Evidence-Based Clinical Practice Guidelines. Chest 2007; 131:4-42
Committee. LungNet, an information service and network of lung support groups was also created,
informed by a Better Breathing Program to assess community-based groups that were set up to promote
self-management and independent living skills in clients with breathing disorders. An informal �Pulmonary
Rehabilitation Network’ of health professionals wishing to share information and knowledge was
established, and in 2004 began the task of developing a PR Toolkit for those wishing to set up or enhance
PR programs (in conjunction with Australian Physiotherapy Association – APA).
Close liaison between the ALF COPD Committee and the Thoracic Society of Australia and New Zealand
(TSANZ) created a TSANZ/ALF COPD Guidelines Steering Group, charged with assembling,
promulgating, implementing and evaluating evidence-based Guidelines for management of COPD
(“COPD-X”TM). The initial version was published in 20037 after considerable consultation and consensus.
An independent ALF Evaluation Committee reviews evidence quarterly, and the COPD-X online version is
updated. A formal Update was print-published in 20068. This PR Manual meshes with these Guidelines.
Given an expanding base of evidence, and a dearth of available programs in Australia, PR has been given
very high priority by the ALF and TSANZ. In 2000 the ALF recommended to the TSANZ that there was a
need for a set of Standards for PR, and a grant was offered under the ALF-Boehringer Ingelheim Award.
The brief was to undertake wide collaboration and a careful search of scientific evidence, and to
incorporate the resulting information into a document of Standards. Further products were to be a Toolkit,
available in print and web-based version for people delivering PR and for those wanting to start a new
program, as well as an evidence-based Manual. A submission has now been made to the Australian
Commonwealth Government by ALF for active support of PR around Australia, and it has been piloting
development of a rural and remote version of pulmonary rehabilitation in Aboriginal communities in
Northern Territory and Western Australia.
Program of Evidence-Based Supports for
Pulmonary Rehabilitation in Australia
Goal
To develop a series of resources for people and organisations wishing to set up, conduct, learn about or take
part in pulmonary rehabilitation in Australia. The minimum resource will be a set of Standards for
Pulmonary Rehabilitation in Australia, but other resources need to be planned:
• a Guidelines document (or �Manual’) based on best available evidence
• a consensus summary document for easy reference
• a toolkit of materials to support developing programs in a range of jurisdictions
• development of a Pulmonary Rehabilitation Database, with emphasis on outcomes
Resources
•
•
•
•
•
•
•
ALF Patient Support Groups (PSG) Needs Analysis (1998)
ALF National Survey of Pulmonary Rehabilitation Programs (1999)
ALF National Consumer Survey of Pulmonary Rehabilitation (2000)
ALF detailed survey of selected pulmonary rehabilitation sites (2000)
AACVPR Guidelines for Pulmonary Rehabilitation Programs (third edition, 2005)
Medline, Embase, Psychlit, CINAHL, Cochrane, and other evidence of effects and cost of Pulmonary
Rehabilitation, and effects and cost of COPD, chronic bronchitis and emphysema (1999, 2001, 2006)
ALF COPD Case Statement and COPD Economic Case Statement
7
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
8
Abramson MJ, Crockett AJ, Frith PA, McDonald CF. COPDX: an update of guidelines for the
management of chronic obstructive pulmonary disease with a review of recent evidence. Med J Aust 2006;
184:342-345
12
•
•
•
•
Guidelines of Management of COPD - TSANZ (�COPD-X’ 2003 and 2006), BTS, NICE, ATS, ERS,
ATS/ERS
Global Initiative on Obstructive Lung Disease Guidelines for Management of COPD (�GOLD’). 2001,
2003, 2006
"Improving Cardiac Care and Outcomes. New South Wales Policy Standards for Cardiac
Rehabilitation". NSW Health Department. State Health Publication No: (C)97 0120.
“Best Practice Guidelines for Cardiac Rehabilitation and Secondary Prevention”. Heart Research
Centre (AJ Goble and MUC Worcester), DHS Victoria (1999)
Stages of Development
F
F
F
F
F
F
F
F
F
F
Search and critically review all available relevant scientific publications about pulmonary
rehabilitation, its components and its links (including patient support).
Evaluate systematic reviews, randomised controlled trials and other research about PR
Develop a package of minimum standards for each component of pulmonary rehabilitation and its
components, documenting strength of supporting evidence, and continually updating them (�A Manual
for Pulmonary Rehabilitation in Australia’, an evidence base for a Pulmonary Rehabilitation Toolkit
o Descriptions and analyses of community-based treatments
o The place of different PR programs in COPD management
o Outcome assessment tools
o Health economics of PR and PSGs
o Role of PR in other respiratory causes of dyspnoea
o Staging of PR and linkages with other therapies
Consult with people and organisations who have published high level research, and with Australian
and New Zealand people and organisations currently undertaking such research.
Review Australian and overseas models (notably home-based/community programs).
Consult with groups providing PR (of various types), or with a particular stake in PR and its place in
community care and disease management of chronic lung diseases.
o Respiratory physicians
o Physiotherapists
o Nurses and asthma educators
o Respiratory scientists
o Exercise rehabilitation scientists
o General practitioners
o Clients, consumers and carers
o Patient support groups
o Other allied health professionals
o Relevant Government and non-government agencies
Provide updated �Summary of evidence-based recommendations’ for ALF web-site
Assist with the development of a �Pulmonary Rehabilitation Toolkit’ by ALF
Circulate draft of �Manual’ to ALF COPD Coordinating Committee, ALF/APA Pulmonary
Rehabilitation Toolkit Steering Committee, ALF COPD-X Evaluation Committee, TSANZ COPD
SIG, TSANZ Executive and other relevant organisations and individuals for final critique
Publish �A Manual for Pulmonary Rehabilitation in Australia’, and update according to emerging high
level evidence at least triennially
Acknowledgements
The Australian Lung Foundation (ALF) has been a tireless and generous investor in the diagnosis and
management of Chronic Obstructive Pulmonary Disease (COPD), and their support for the Pulmonary
Rehabilitation Toolkit Program is applauded. The ALF National Council accepts the importance of patient
support and the central role of pulmonary rehabilitation for people with chronic and complex respiratory
diseases, and determined that its annual ALF-Boehringer Ingelheim Australia Award should be directed to
the support of this project. The ALF COPD Coordinating Committee gave oversight. L Thompson, G Perl,
W Darbishire, H Allen and D Marshall have been vital supporters.
13
Critical reviews of medical literature have been vital. P Walker, A Crockett and J Cranston provided
invaluable assistance in its first and second iterations. P Cafarella and J Duffy have subsequently helped
review psychological comorbidities and treatments. D Schembri has provided physiological contributions,
and T Hunt has helped review trials of heliox supplementation. K Humphrys and G Cross have contributed
expert nutritional advice and literature reviewing. Pulmonary rehabilitation programs around Australia, and
data from the ALF Better Breathing initiative have also provided valuable information. In particular, J
Allison, L Spencer and S Jenkins have been critical in early surveys and creation of the Pulmonary
Rehabilitation Toolkit. Many individuals and organisations prepared superb expressions of interest, which
are acknowledged. Ideas gathered from people with COPD and other chronic and complex respiratory
conditions are too countless to mention. It would be unfair to single out individuals, but thanks to you all!
Medical staff in the Repatriation General Hospital (RGH) and Southern Respiratory Services (SRS) have
been generous in backfilling time for this lengthy project, and with its literature searching and revision. B
Hamilton, K Hendra and S Spry have helped with word processing advice and protecting my time.
I hope this Manual - the outcome of the energies and supports of many people - is a helpful reference work
for ongoing enhancement of Pulmonary Rehabilitation in Australia. The ultimate acknowledgement must
be to those who use this document and its associated Toolkit for the well-being of those many hundreds of
thousands of Australians suffering from chronic respiratory diseases.
Peter Frith. July 2008
14
2. DEFINITIONS AND
DESCRIPTIONS
2.1 Chronic Obstructive Pulmonary Disease
(COPD)
The most widely recognised working definition of COPD is that adopted by the Global Initiative
for Chronic Obstructive Lung Disease (GOLD):
"COPD is a disease state characterized by poorly reversible airflow
limitation that is usually progressive and associated with an abnormal
inflammatory response of the lung to noxious particles or gases,
particularly cigarette smoke. Symptoms, functional abnormalities, and
complication of COPD can all be explained on the basis of this
underlying inflammation and resulting pathology."9,10
The term COPD has globally superseded use of such terms as chronic airflow limitation (CAL),
chronic obstructive airways (or lung) disease (COAD or COLD) and chronic airways obstruction
(CAO).
COPD is an acquired inflammatory and degenerative condition of the lungs. The inflammatory
nature of the condition, with its pulmonary and systemic ramifications, has been described11, with
a recent update12. The effects of inflammation and the syndrome of COPD are unstable but
ultimately progressive. The natural rate of decline of lung function (FEV1) after 25 years of age is
15 to 30 mL per year. In �susceptible’ smokers who continue to smoke, however, the decline
averages 60 mL per year and may be as great as 200 mL per year.
Greater emphasis is now placed on the preventability and treatability of COPD - rather than
earlier descriptions of it being incurable13,14 - as is the case with chronic heart failure, diabetes,
depression, chronic renal disease and many other chronic conditions.
9
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
10
Rabe KF, Hurd S, Anzueto A, et al. Global strategy for the diagnosis, management, and prevention of
COPD: GOLD executive summary. Am J Respir Crit Care Med 2007; 176:532-555
11
Wouters EFM. Local and systemic inflammation in chronic obstructive pulmonary disease. Proc Am
Thorac Soc 2005; 2:26-33
12
Wouters EFM, Groenewegen KH, Dentener MA, Vernooy JHJ. Systemic inflammation in chronic
obstructive pulmonary disease. Proc Am Thorac Soc 2007; 4:626-634
13
Fabbri LM, Hurd SS. Global strategy for the diagnosis and management and prevention of COPD. 2003
Update. Eur Respir J 2003; 22:1-2
14
National Collaborating Centre for Chronic Conditions. Chronic obstructive pulmonary disease. National
clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and
secondary care. Thorax 2004; 59(Suppl 1):1-232
15
Those who stop smoking during their 40’s still have a greater rate of functional decline than nonsmokers, albeit slower than continuing smokers15,16,17. Airway and systemic inflammation are
associated with more rapid decline in lung function, as well as other poor outcomes, and are
increased by exacerbations of the disease18.
In essence COPD is more a syndrome than a specific disease, as there are different
pathophysiologies and clinical presentations. The typical phenotypes are emphysema and
chronic bronchitis, though bronchiectasis and chronic asthma can also be identified in many
patients. Chronic lung inflammation triggered by noxious inhalants appears to result from damage
to the innate immune system in some individuals, with imbalances within protease-antiprotease
and oxidative stress-antioxidant mechanisms, and ultimately leads to widespread pathological
changes that represent COPD. The debate around whether these changes occur only in a
proportion of �susceptible’ individuals is resolving19. Central and peripheral airway inflammation,
oedema, mucus hyper-secretion, and ciliary dysfunction can lead to airway obstruction, airflow
limitation, sputum production and dilation and destruction of respiratory bronchioles and alveoli.
Fixation of airflow limitation arises from remodelling of small airways and loss of elastic support
of airway walls when there is emphysema. Despite the traditional view of irreversible airflow
limitation being the physiological feature of COPD, it is increasingly recognised that there is a
range of bronchodilator responsiveness, blurring the distinction between asthma and COPD20,21.
The diagnosis of COPD relies on the identification of airflow limitation that is not reversible or at
best only partially reversible following bronchodilator22,23. A fixed ratio for FEV1/FVC of 0.70 is
the cut-off value recommended, although arguments have been put that this underestimates
COPD in younger people and overestimates in older people24. It is recognised that FVC may be
difficult for some untrained people to achieve, and the FEV6 (forced expired volume in six
seconds) has been suggested as a replacement for the FVC, and hence the FEV1/FEV6 ratio has
emerged25,26,27. This has been tested in and Austrian population-based study (n=1,349), and its
15
Fletcher C, Peto R. The natural history of chronic airflow obstruction. Brit Med J 1977; 1:1645-1648
Anthonisen NR, Connett JE, Kiley JP, Altose MD, et al. Effects of smoking intervention and the use of
an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA
1994; 272:1497-1505
17
Anthonisen NR, Connett JE, Murray RP. Smoking and lung function of Lung Health Study participants
after 11 years. Am J Respir Crit Care Med 2002; 166:675-679
18
Donaldson GC, Seemungal TAR, Patel IS, Bhowmik A, et al. Airway and systemic inflammation and
decline in lung function in patients with COPD. Chest 2005; 128:1995-2004
19
Vestbo J, Hogg JC. Convergence of the epidemiology and pathology of COPD. Thorax 2006; 61:86-88
20
Tashkin DP, Celli B, Decramer M, Liu D, et al. Bronchodilator responsiveness in patients with COPD.
Eur Respir J 2008; 31:742-750
21
Soriano JB, Mannino DM. Reversing concepts on COPD reversibility. Eur Respir J 2008; 31:695-696
22
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
23
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
24
Celli BR, Halbert RJ, Isonaka S, Schau B. population impact of different definitions of airways
obstruction. Eur Respir J 2003; 22:268-273
25
Vandevoorde J, Verbanck S, Schuermans D, et al. FEV1/FEV6 and FEV6 as an alternative for
FEV1/FVC and FVC in the spirometric detection of airways obstruction and restriction. Chest 2005;
127:1560-1564
26
Hansen JE, Sun X-G, Wasserman K. Should forced expiratory volume in six seconds replace forced vital
capacity to detect airways obstruction? Eur Respir J 2006; 27:1244-1250
16
16
sensitivity for airflow limitation was high when a low FEV1 value was included in the
algorithm28.
There has been substantial discussion about the merits or otherwise of early diagnosis utilising
spirometry in primary care29. The FEV1/FEV6 ratio has a potential advantage of being
measurable using inexpensive and simple equipment and this may lend itself to case-finding or
screening for early diagnosis. On the other hand opinions are divided on whether it is useful and
cost-effective to make earlier diagnoses. The findings from a survey in a working population in
France (n=5,008) that even mild COPD is associated with significant dyspnoea and impairments
in quality of life30, and, from other studies, that early identification of airflow limitation assisted
with smoking cessation31,32 provide encouragement to diagnose COPD earlier in its trajectory.
Increasing use of spirometry in primary care is feasible33. GP use of electronic spirometers in
patients aged 35-70 (n=3,408) detected 126 new patients, of whom 42% would have been missed
by a screening questionnaire34. In a combined questionnaire and spirometry screening study in
Belgian general practices there was a high new case detection rate35. Open-access spirometry tests
made available to a local area resulted in a new diagnosis of COPD for over 40% of those with
full results, and they were considered to be under-treated before testing36. Despite these positive
findings, however, a number of problems associated with primary care spirometry have been
identified. In Australia, for example (and similar trends have been seen in other countries), as
many as three-quarters of GPs own an electronic spirometer but infrequently use them, and of
those who do, low numbers perform high quality measurements or maintain their equipment
adequately37. Barriers to more widespread use relate to organisational and technical difficulties as
well as poor understanding of interpretation of results and the clinical value of the test38. Training
27
Akpinar-Elci M, Fedan KB, Enright PL. FEV6 as a surrogate for FVC in detecting airways obstruction
and restriction in the workplace. Eur Respir J 2006; 27:374-377
28
Lamprecht B, Schirnhofer L, Tiefenbacher F, et al. Six-second spirometry for detection of airway
obstruction. A population-based study in Austria. Am J Respir Crit Care Med 2007; 176:460-464
29
Enright PL, Crapo RO. Controversies in the use of spirometry for early recognition and diagnosis of
chronic obstructive pulmonary disease in cigarette smokers. Clin Chest Med 2000; 21:645-652
30
Roche N, Dalmay F, Perez T, et al. Impact of chronic airflow obstruction in a working population. Eur
Respir J 2008; 31:1227-1233
31
Clotet J, Gomez-Arbones X, Ciria C, Albalad JM. Spirometry is a good method for detecting and
monitoring chronic obstructive pulmonary disease in high-risk smokers in primary health care. Arch
Bronconeumol 2004; 40:155-159
32
Bednarek M, Gorecka D, Wielgomas J, et al. Smokers with airway obstruction are more likely to quit
smoking. Thorax 2006; 61:869-873
33
Griffiths C, Feder G, Wedzicha J, et al. Feasibility of spirometry and reversibility testing for the
identification of patients with chronic obstructive pulmonary disease on asthma registers in general
practice. Respir Med 1999; 93:903-908
34
Buffels J, Degryse J, Heyrman J, Decramer M. Office spirometry significantly improves early detection
of COPD in general practice. The DIDASCO Study. Chest 2004; 125:1394-1399
35
Vandevoorde J, Verbanck S, Gijssels L, et al. Early detection of COPD: A case finding study in general
practice. Respir Med 2007; 101:525-530
36
Walker PP, Mitchell P, Diamantea F, et al. Effect of primary care spirometry on the diagnosis and
management of COPD. Eur Respir J 2006; 28:945-952
37
Johns DP, Burton D, Walters JAE, Wood-Baker R. National survey of spirometer ownership in general
practice in Australia. Respirology 2006; 11:292-298
38
Walters JAE, Hansen E, Mudge P, et al. Barriers to the use of spirometry in general practice. Aust Family
Phys 2005; 34:1-3
17
has been shown to increase GPs’ use39 and accuracy40 of spirometry. Computerised expert
interpretations have been evaluated, although with disappointing results41.GP training in
spirometry has therefore been attempted, using a range of methods, with relatively poor success
in improving quality or rates of use unless quite intensive efforts are made42, including refresher
sessions. Educational outreach visits add further value43, especially with individually tailored
feedback44.
The relative value and accuracy of using questionnaires or spirometry for case-finding has been
discussed. Diagnostic questionnaires have been developed and validated45,46, with somewhat
disparate findings47, using laboratory-based spirometry as the diagnostic reference point.
FEV1/FEV6 using simple measurement tools has also been validated against high quality
spirometry, and has very high validity and utility48. In this same study, simple flow measurement
was superior to the questionnaires for case finding.
Airflow limitation leads to static lung overinflation with increased work of breathing. During
activities, the physical work leads to increased ventilation, and lung units with greatest airway
narrowing are unable to empty at higher flow rates. This results in uneven ventilation and
emptying which in turn lead to both increased mis-matching of ventilation and perfusion and also
dynamic hyperinflation. The work of breathing therefore increases dramatically, and gas
exchange inefficiency may also cause oxygen desaturation, either or both of which result in
dyspnoea, the prime clinical characteristic of COPD.
Systemic manifestations, related to muscles, heart, body composition, and mental health must be
accounted for in disease management.
Small vessel vasculitis is also often seen, and in combination with ventilation maldistribution,
contributes to gas exchange abnormalities that result in hypoxaemia. This in turn can lead to
further pulmonary vasoconstriction and ultimately pulmonary hypertension.
It needs to be emphasised that COPD is a largely preventable condition (cigarette smoke,
occupational exposures, poor control of asthma, and indoor and outdoor air pollution are the
leading aetiologic factors). Primary prevention needs to be promoted at all opportunities by PR
39
O’Dowd LC, Fife D, Tenhave T, Panettieri RA. Attitudes of physicians toward objective measures of
airway function in asthma. Am J Med 2003; 114:391-396
40
Bellia V, Pistelli R, Catalano F, et al. Quality control of spirometry in the elderly. The S.A.R.A study.
Am J Respir Crit Care Med 2000; 161:1094-1100
41
Poels PJP, Schremer TRJ, Schellekens DPA, et al. Impact of a spirometry expert system on general
practitioners’ decision making. Eur Respir J 2008; 31:84-92
42
Eaton T, Withy S, Garrett JE, et al. Spirometry in primary care practice: the importance of quality
assurance and the impact of spirometry workshops. Chest 1999; 116:416-423
43
Thuyns AV, Schermer TRJ, Jacobs JE, et al. Effect of periodic outreach visits by lung function
technicians on the validity of general practice spirometry. Eur Respir J 2003; 22:439s
44
Tomson O’Brien MA, Oxman AD, Davis DA, et al. Educational outreach visits: effects on professional
practice and health care outcomes. Cochrane Database Syst Rev 2002, Issue 2:CD000409
45
Price DB, Tinkelman DG, Halbert RJ, et al. Symptom-based questionnaire for identifying COPD in
smokers. Respiration 2006; 73:285-295
46
Tinkelman DG, Price DB, Nordyke RJ, et al. Symptom-based questionnaire for differentiating COPD
and asthma. Respiration 2006; 73:296-305
47
Kotz D, Nelemans P, van Schayck CP, Wesseling GJ. External validation of a COPD diagnostic
questionnaire. Eur Respir J 2008; 31:298-303
48
Frith P, Crockett AJ, Beilby J, et al. Validation of a simple device to screen for COPD in primary care.
Submitted.
18
practitioners, as well as secondary prevention, in order to reduce airway inflammation and its
consequences. Therapies that reduce airway and systemic inflammation and their consequences,
dilate and stabilise airways with the goal of deflating hyperinflated lungs, and enhance and
maintain exercise capacity through good nutrition and exercise training are likely to improve
overall health status, mood and carer health, and reduce exacerbations and mortality. The
complex comorbidities of COPD need also to be taken into account when assessing and treating
COPD, in line with evolving appreciation of chronic disease management. This Manual therefore
provides substantial background material to help practitioners understand COPD and its
implications elsewhere.
2.2 Clinical Indicators and Outcome
Measures
Public accountability for clinical practice has challenged health professionals to be more
systematic in documenting clinical outcomes, and the ability to assemble and analyse data has
enabled professionals to turn this need into a science. As clinical practice has been more minutely
examined, and clinical outcomes more readily measured, variations in both practice and outcomes
have emerged. It has been stated, though, that “there are enough outcome measures and tests
available to keep both the patient and the pulmonary rehabilitation staff busy for the entire
rehabilitation time period!”49, and some rationality is needed.
The impacts of interventions are termed outcomes, so assessment of outcomes should be an
integral part of good clinical practice. This Manual does not cover all possible measures, but most
of those reported in trials of PR are addressed. Recommendations for using particular measures
are based on evidence for their utility and validity. Recent publications have provided
comprehensive discussion of a wide range of outcomes measures of potential use in trials of drug
therapies50, and a prospective study of what measures most effectively predict long term disease
outcome is currently underway51. These articles are recommended for careful consideration.
Health outcomes
Health outcomes may relate to impairments, disabilities, handicaps and costs. Outcome
measures should be accurate, relevant to the intervention, reliable, and have undergone careful
validation. For health outcomes to result in changes in clinical practice they should be overtly
relevant to the clinical problem, and address consumer satisfaction, patient preferences and
community needs.
It is useful to distinguish between effectiveness and efficacy of specific interventions.
•
Effectiveness refers to benefits observed from an intervention in a real-life setting with
unselected clinic patients, staff of average capability, and in facilities with real-life levels
of funding.
49
ZuWallack RL. Outcome measures for pulmonary rehabilitation. Eur Respir Monograph 2000; 5:177200
50
Cazzola M, MacNee W, Martinez FJ, et al. ATS/ERS Task Force. Outcomes for COPD pharmacological
trials: from lung function to biomarkers. Eur Respir J 2008; 31:416-468
51
Vestbo J, Anderson W, Coxson HO, et al. Evaluation of COPD longitudinally to identify predictive
surrogate end-points (ECLIPSE). Eur Respir J 2008; 31:869-873
19
•
Efficacy is determined in research trials, preferably randomised controlled trials, with
carefully selected patients, usually highly qualified, specifically employed and motivated
staff, in well-equipped research facilities.
Health Economic Outcomes
It is increasingly acknowledged that economic issues are also important52. Little work had been
done before 1990 in either COPD or asthma53, but analyses are increasingly applied in research
trials, and certainly in evaluating clinical programs when sustainability issues arise. A useful
review of health economics in COPD was recently published by Halpin.54
•
Cost-benefit analysis assesses which of two treatment programs is the more beneficial in
terms of resources saved versus resources used. Both the costs and the benefits are expressed
in dollar terms. Improvements in productivity may enhance the cost-benefit of a particular
treatment. Such analysis does not account for the value placed by society or the individual on
achieving certain outcomes at stated costs.
•
Incremental cost-benefits provide an understanding of the marginal cost of adding one type
of intervention to another (e.g. adding an education program to an exercise program in PR).
If a treatment provides benefits that are delayed for a year or more after an immediate cost is
incurred, a discount is applied to the delayed benefits, at an agreed rate (e.g. 5% per annum),
so treatments with different time-frames can be compared.
•
Cost-effectiveness analysis determines which of two alternative interventions offers the
lowest cost per unit of benefit. It evaluates a ratio of total costs (numerator) to effectiveness
(denominator). The costs are those related to the interventions studied minus savings accruing
through prevention of events. The costs of two interventions (e.g. PR vs lung volume
reduction surgery) may therefore be compared to their respective consequences. The
outcomes need to be measured in the same units, and all resource implications (costs) are
considered, including opportunity costs (related to spreading fixed funding between different
programs and opportunities surrendered when one program is supported over another). Most
commonly effectiveness is expressed as increased years of life, though it may be related to
the number of lives saved or other outcomes. Cost-effectiveness is therefore expressed as a
net cost per net outcome (cost-effectiveness ratio), and it indicates which intervention
provides more value for money. A more expensive intervention may be more value than a
less expensive one because its clinical effectiveness is substantially greater.
• Cost-utility analysis is a variant of cost-effectiveness analysis, in which outcomes as
consequences of interventions are expressed in utilities (eg QALYs and DALYs) instead of
natural units. The QALY (Quality-Adjusted Life Year) and DALY (Disability Adjusted Life
Year) are the best-known measures of utility; they are based on a quantity of life scale
adjusted for its quality.
52
Drummond MF, Stoddard G, Torrance GW. Methods for the economic evaluation of health care
programmes. Critical assessment of economic evaluation. Oxford: Oxford University Press 1987
53
Molken MP, van Doorslaer EK, Rutten FF. Economic appraisal of asthma and COPD care: a literature
review 1980-1991. Soc Sci Med 1992; 35:161-175
54
Halpin DMG. Health economics of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2006;
3:227-233
20
Indicators of Respiratory Impairment
Measures from Static Respiratory Tests
In each case, methodological details are addressed in Chapter 6. The tests have been developed
and standardised over many years, and have value in describing respiratory impairment. There are
ATS/ERS55 and TSANZ Standards that apply56 to testing and interpretation57.
Spirometry requires maximum effort from the patient and standardised performance by the
person supervising the test (Table 2.1). Some patients are unable to provide satisfactory results.
However, results have major prognostic significance and are clinically meaningful. Moreover,
spirometry results are a requirement for diagnosis and assessment of severity in COPD; the
bronchodilator responsiveness of spirometry also helps in the differential diagnosis from asthma,
and the patterns of results help to distinguish COPD from interstitial lung disorders.
Other tests of lung function not requiring forced expiratory effort have been developed, such as
forced and impulse oscillometry58,. They may provide interesting research questions, but are not
yet applicable to routine clinical assessment. Estimation of subdivisions of lung volumes (gas
dilution or body plethysmography) helps document the work of breathing influenced by gas
trapping and overinflation (Table 2.2). Gas transfer measurements, using carbon monoxide as the
indicator gas, help in understanding the anatomic cause of dyspnoea (Table 2.3).
TABLE 2.1.
FEV1
FEV1/FVC
FVC
SVC
MEASURES FROM SPIROMETRY59,60,61,62
Volume (litres) exhaled in the first second of a forced expiration from TLC.
Normal values are determined from patient race, gender, age and height.
Lower limit of normal (2 standard deviations) should be used to delineate abnormal results, but where
LLN is not easily ascertained, 80% is a reasonable approximation.
Ratio of FEV1 to FVC. Normally over 75% of the FVC is exhaled in one second, so ratios below 0.70
indicate airflow limitation.
Total volume (litres) exhaled over a forced expiration from TLC to RV.
Normal values are determined from patient race, gender, age and height.
Values < 80% of predicted are abnormal.
Total volume (litres) exhaled over a full slow expiration from TLC to RV.
Normal values determined from race, gender, age height, and values below 80% of predicted are
abnormal.
SVC is usually higher than FVC, as forced expiration causes dynamic airway compression.
55
Miller MR, Crapo RO, Hankinson J, Brusasco V, et al. General considerations for lung function testing.
Eur Respir J 2005; 26:153-161
56
Pierce RJ, Hillman D, Young IH, et al. Respiratory function tests and their application. Respirology
2005; 10:S1-S19
57
Pellegrino R, Viegi G, Brusasco V, Crapo R, et al. Interpretative strategies for lung function tests. Eur
Respir J 2005; 26:948-968
58
Smith HJ, Reinhold P, Goldman HD. Forced oscillation technique and impulse oscillometry. Eur Respir
Mono 2005; 31:72-105
59
Quanjer PH, Tammeling GJ, Cotes JE, Pedersen OF, et al. Lung Volumes and forced ventilatory flows.
Report Working Party. Standardization of lung function tests. European Community for Steel and Coal.
Eur Respir J 1993; 6 (Suppl 16):5-40
60
Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories (Crapo RO,
Chairman). Standardization of spirometry; 1994 update. Am J Respir Crit Care Med 1995; 152:1107-1136
61
Miller MR, Crapo RO, Hankinson J, Brusasco V, et al. General considerations for lung function testing.
Eur Respir J 2005; 26:153-161
62
Pierce RJ, Hillman D, Young IH, et al. Respiratory function tests and their application. Respirology
2005; 10:S1-S19
21
TABLE 2.2.
TLC
RV
RV/TLC
TV
IC and
IC/TLC
TABLE 2.3.
DLCOSB or
TLCOSB
MEASURES FROM BODY PLETHYSMOGRAPHY OR INERT GAS DILUTION63,64,65,66
Total lung capacity (litres). The overall volume of air within the lungs after a full inhalation. [TLC =
RV + SVC, or TLC = FRC + IC].
Normal values are determined from race, gender, age and height.
Values < 80% of predicted are abnormal.
Low values indicate restriction (e.g. pulmonary fibrosis, lung resection, pleural disease, chest wall
disease or obesity).
Values > 120% of predicted are also abnormal, and indicate static hyperinflation.
Residual volume (litres). The amount of air left within the lungs after a full expiration.
Normal values are determined from race, gender, age and height.
Values < 80% of predicted are abnormal.
Low values occur with restriction (e.g. pulmonary fibrosis, lung resection, pleural disease, chest wall
disease or obesity).
Values > 120% of predicted are also abnormal, and occur with air-trapping (e.g. from persistent
airway narrowing).
Ratio of RV : TLC.
Normal values depend mainly on age.
Values over 120% of predicted are abnormal, and indicate distal air-trapping (e.g. from persistent
airway narrowing)
Tidal volume (litres). The volume of air breathed during normal resting breaths.
Inspiratory capacity (litres).The volume difference between FRC and TLC.
IC/TLC is reduced where there is air-trapping.
MEASURES FROM CARBON MONOXIDE GAS TRANSFER TEST67,68,69,70
Gas transfer or transfer factor (mL CO per second per mmHg). The amount of carbon monoxide
removed from a full inhalation of air containing trace quantities of carbon monoxide.
Reflects gas transfer across the alveolar membranes from alveolar air to red cells haemoglobin.
Normal values depend on race, gender, age, height, and haemoglobin level.
Values < LLN (or < 80% of predicted), after correction for haemoglobin levels, are abnormal, and
indicate abnormal gas exchange (e.g. from pulmonary fibrosis or other interstitial lung disease,
emphysema, or pulmonary vascular disease).
Values above the upper limit of normal (ULN), or > 120% of predicted may be abnormal, and occur
where there is high circulating blood volume or intrapulmonary haemorrhage (e.g. Goodpasture's
syndrome).
63
Coates AL, Peslin R, Rodenstein D, Stocks J. Measurement of lung volumes by plethysmography. Eur
Respir J 1997; 10:1415-1427
64
Brown R, Leith DE, Enright PL. Multiple breath helium dilution measurement of lung volumes in adults.
Eur Respir J 1998; 11:246-255
65
Stocks J, Quanjer PH. Reference values for residual volume, functional residual capacity and total lung
capacity. ATS Workshop on Lung Volume Measurements. Eur Respir J 1995; 8:492-506
66
Wanger J, Clausen JL, Pedersen OF, et al. Standardisation of the measurement of lung volumes. Eur
Respir J 2005; 26:511-522
67
Cotes JE, Chinn DJ, Quanjer PH, Roca J, Yernault J-C. Standardization of the measurement of transfer
factor (diffusing capacity). Report Working Party. Standardization of lung function tests. European
Community for Steel and Coal. Eur Respir J 1993; 6 (Suppl 16):41-52
68
American Thoracic Society. Single breath carbon monoxide diffusing capacity (transfer factor). Am Rev
Respir Dis 1987; 136:1299-1307
69
Pierce RJ, Hillman D, Young IH, et al. Respiratory function tests and their application. Respirology
2005; 10:S1-S19
70
MacIntyre N, Crapo RO, Viegi G, Johnson DC, et al. Standardisation of the single-breath determination
of carbon monoxide uptake. Eur Respir J 2005; 26:720-735
22
Measures from Functional Tests
Functional tests reflect a person’s ability to undertake activity of daily living. They are simple to
conduct, though some training is required. A systematic overview suggested that the 6-minute
walk is the test of choice as a functional test in both clinical and research settings71.
TABLE 2.4.
WALKING TESTS
6-minute walk test
Shuttle walk test
Walking endurance
tests
Self-paced distance (metres) walked in 6 minutes, along a standard course, with
standard encouragement72,73.
Normal values relate to age and gender.
Clinically significant changes are inferred from changes > 49 m.
Distance (metres) walked in an incremental test to exhaustion, over a standard
circuit, with standard encouragement74.
Normal values relate to age and gender.
Time of walking at a set pace based on maximum walking capacity.
May be done on a treadmill or a Shuttle test circuit75.
Complex exercise tests have been more relevant to research as they require expensive equipment
with highly skilled scientist involvement and physician interpretation, although with
technological advances, they are emerging as useful clinical tools. They can assist in determining
the cause of limitation, and therefore help target therapies more effectively. They can also provide
valuable information about endurance, which in turn can help in prescribing exercise training
loads. They can also provide a number of highly relevant outcome measures.
TABLE 2.5.
Type of test
Incremental
ergometry
Steady-State
tests
ERGOMETER TESTS76
Description of test
Performed on treadmill or cycle
ergometer. Initial values at rest,
then unloaded exercise, then
increasing load to exhaustion (i.e.
symptom-limited maximum test). .
Many others are calculated.
Exercise on cycle or treadmill
ergometer at specific levels of work
usually determined from
incremental ergometry.
Measurements
VE
HR
VO2
VCO2
W
Explanation
ventilation (litres)
heart rate (beats per min)
oxygen uptake (mL/min)
carbon dioxide uptake (mL/min)
workload (watts)
Reasons for tests:
Study cardiovascular and metabolic functions under load
•
a standard measure of endurance
•
a provocation for exercise-induced asthma77
71
Solway S, Brooks D, Lacasse Y, Thomas S. A qualitative systematic overview of the measurement
properties of functional walk tests used in the cardiorespiratory domain. Chest 2001; 119:256-270
72
McGavin CR, Gupta SR, McHardy GJR. Twelve-minute walking test for assessing disability in chronic
bronchitis. Br Med J 1976; 1:822-823
73
Butland RJ, Pang J, Gross ER, Woodcock AA, Geddes DM. Two-, six-, and 12-minute walking tests in
respiratory disease. Brit Med J 1982; 284:1607-1608
74
Singh SJ, Morgan MDL, Scott S, Walters D, Hardman AE. Development of a shuttle walking test of
disability in patients with chronic airways obstruction. Thorax 1992; 47:1019-1024
75
Revill SM, Morgan MDL, Singh SJ, Williams J, Hardman AE. The endurance shuttle walk: a new field
test for the assessment of endurance capacity in chronic obstructive pulmonary disease. Thorax 1999;
54:213-222
76
ERS Task Force on Standardization of Clinical Exercise Testing. Clinical exercise testing with reference
to lung diseases. Indications, standardization, and interpretation strategies. Eur Respir J 1997; 10:16621689
77
American Thoracic Society. Guidelines for methacholine and exercise challenge testing. Am J Respir
Crit Care Med 2000; 161:309-329
23
Indicators of Psychological Impairment
There is increasing evidence supporting the importance of psychological impairments in chronic
lung disease, though the epidemiology related to their prevalence and burden is inconsistent.
Different interpretations may be driven most by the population under examination, with
psychological distress being more prevalent in people with more severe disease. Further,
confusion between psychological distress and mental health disorders exists, and needs to be
clarified.
Apart from the population being investigated, another problem with estimating prevalence of
mood disorders in people with COPD (and their carers) is the variety of measurement tools used.
These vary from broad-based psychological health/distress questionnaires to specific anxiety or
depression inventories and structured interviews for a codable psychiatric diagnosis. These issues
are considered in more detail in the discussion of specific outcome measures.
Indicators of Nutritional Impairment
People with COPD develop an increasing potential for a variety of nutritional impairments and
changes in body composition as the disease progresses. Weight loss, in particular, is seen in a
third or more of those with moderate-to-severe COPD78,79,80,81. Nutritional impairments may have
significant effects on ability to function in everyday life. Those who are underweight have
impaired exercise tolerance82,83, and there is a close association between nutritional depletion and
quality of life84,85. Moreover, worse nutritional status is associated with higher mortality
78
Engelen MPKJ, Schols AMWJ, Baken WC, et al. Nutritional depletion in relation to respiratory and
peripheral skeletal muscle function in outpatients with COPD. Eur Respir J 1994; 7:1793-1797
79
Braun SR, Keim NL, Dixon RM, Clagnaz P, et al. The prevalence and determinants of nutritional
changes in chronic obstructive pulmonary disease. Chest 1984; 86:558-563
80
Schols AMWJ, Soeters PB, Dingemans AMC, Mostert R, et al. Prevalence and characteristics of
nutritional depletion in patients with stable COPD eligible for pulmonary rehabilitation. Am Rev Respir Dis
1993; 147:1151-1156
81
De Benedetto F, Del Ponte A, Marinari S, Spacone A. In COPD patients, body weight excess can mask
lean tissue depletion: a simple method of estimation. Monaldi Arch Chest Dis 2000; 55:273-278
82
Baarends EM, Schols AM, Mostert R, Wouters F. Peak exercise response in relation to tissue depletion
in patients with chronic obstructive pulmonary disease. Eur Respir J 1997; 10:2807-2813
83
Kobayashi A, Yoneda T, Yoshikawa M, Ikuno M, et al. The relation of fat-free mass to maximum
exercise performance in patients with chronic obstructive pulmonary disease. Lung 2000; 178:119-127
84
Shoup R, Dalsky G, Warner S, Davies M, et al. Body composition and health-related quality of life in
patients with obstructive airways disease. Eur Respir J 1997; 10:1576-1580
85
Mostert R, Goris A, Weling-Scheepers C, et al. Tissue depletion and health related quality of life in
patients with chronic obstructive pulmonary disease. Respir Med 2000; 94:859-867
24
rates86,87,88,89 in patients with moderate to severe COPD, and this has been replicated in people
with severe COPD requiring long-term oxygen therapy90.
Body mass and body composition may have different implications. Body mass index (BMI) is a
function simply of height and weight (weight in Kg / [height in metres]2), and includes fat and
fat-free mass; significant muscle wasting can occur in people with normal or even high BMI.
BMI is a strong independent predictor of survival in COPD91,92., . BMI is an independent
indicator of outcome, and has been included in a general impairment index, the BODE Index93,
which has even greater prognostic power in COPD.
Indicators that reflect muscle mass depletion have appeal over BMI as this appears to be the main
component of body mass contributing to the associations with exercise limitation, quality of life
and mortality. Both screening tools and direct measures of fat-free or muscle mass are available.
Patients with COPD whose lean body mass (FFM) is depleted have the greatest impairment of
HRQoL94. Even in COPD patients with normal BMI, FFM was an independent predictor of
mortality95.
Activities of Daily Living
The quality of life for people with moderate and severe COPD is impaired in most aspects of
functioning, from basic self-care, home management, social interactions, to recreational and
leisure activities. The activities of daily living (ADLs) should therefore be a focus of assessment
and for management strategies in disabled patients with COPD. Assessment requires history
taking (which allows appreciation of cognitive capability and interaction with spouse or carer,
self confidence and motivation) and formal functional assessments, by questionnaire and task
performance. Dyspnoea questionnaires, satisfaction with performance scales, and subjective
rating scales are available. Technological advancements are increasingly being applied to the
continuous monitoring of activity like pedometers, accelerometers and other related devices.
86
Wilson DO, Rogers RM, Wright EC, Anthonisen NR. Body weight in chronic obstructive pulmonary
disease. The National Institutes of Health Intermittent Positive-Pressure Breathing Trial. Am Rev Respir Dis
1989; 139:1435-1438
87
Schols AM, Slangen J, Volovics L, Wouters EF. Weight loss is a reversible factor in the prognosis of
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157:1791-1797
88
Schols AMWJ, Broekhuizen R, Weling-Scheepers CA, Wouters EF. Body composition and mortality in
chronic obstructive pulmonary disease. Am J Clin Nutr 2005: 82:53-59
89
Vestbo J, Prescott E, Almdal T, Dahl M, et al. Body mass, fat-free body mass, and prognosis in patients
with chronic obstructive pulmonary from a random population sample. Findings from the Copenhagen
City Heart Study. Am J Respir Crit Care Med 2006: 173:79-83
90
Chailleux E, Laaban J-P, Veale D. Prognostic value of nutritional depletion in patients with COPD
treated by long-term oxygen therapy: data from the ANTADIR Observatory. Chest 2003; 123:1460-1466
91
Gray-Donald K, Gibbons L, Shapiro SH, et al. Nutritional status and mortality in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 1996; 153:961-966
92
Landbo C, Prescott E, Lange P, et al. Prognostic value of nutritional status in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 1999; 160:1856-1861
93
Celli BR, Cote CG, Marin JM, Casanova C, et al. The body-mass index, airflow obstruction, dyspnea,
and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med 2004; 350:1005-1012
94
Mostert R, Goris A, Weling-Scheepers C, et al. Tissue depletion and health related quality of life in
patients with chronic obstructive pulmonary disease. Respir Med 2000; 94:859-867
95
Vestbo J, Prescott E, Almdal T, Dahl M, et al. Body mass, fat-free mass, and prognosis in patients with
chronic obstructive pulmonary disease from a random population sample. Findings from the Copenhagen
City Heart Study. Am J Respir Crit Care Med 2006; 173:79-83
25
While some of this testing is in the realm of exercise scientists and physiotherapists, full
functional assessment and goal-setting is ideally undertaken by interaction between the
physiotherapist and occupational therapist as well as the wider interdisciplinary team. The
primary goal of the occupational therapist is to restore independence in performing ADLs.
Minimising dyspnoea during activities by simplifying tasks may seem to be at odds with the
desire to stimulate cardiovascular training through moderate and high intensity exercise. Balances
and compromises are often needed, and collaboration between patient / carer and the
physiotherapist, exercise scientist and occupational therapist is essential.
Quality of Life
The concept of quality of life (QoL) is complex, and the term is difficult to define, but in essence,
quality of life is best understood as �happiness’. If the main aim of treatment is to reduce
symptoms (dyspnoea, discomfort, pain, misery, and suffering) then standard methods that employ
measurement of impairments may be less relevant to the individual than assessments that reflect
or measure happiness.
A person's standing in relation to a series of core social concerns has been used by the OECD to
define QoL96, with regard to community perceptions of health, education, employment, safety,
justice, leisure time use, participation and social opportunity. Use of objective natural science
indicators, where the patient is considered in isolation from the social milieu, is difficult and
ineffective in evaluating QoL. Subjective QoL, which includes happiness, life satisfaction and
well-being, humanistic characteristics that are critically dependent on stable positive
relationships, is a more reliable measure of QoL97 in health terms.
Health Status
Quality of life is a personal attribute, while health status is a measurable attribute of a population
group98. The most enduring, though crudest, measure of health status of a population is cause of
death obtained from death certificates, but as increased survival rates from chronic diseases occur
so disability assumes increasing importance99. The disability-adjusted life year (DALY) is a
useful measure, as it represents the gap between a population's health status and that of an
optimum reference population100. Just as individual QoL can be assessed from a careful clinical
history, objective health status measures formalise similar questions that assess impacts of disease
on groups of patients and changes following interventions. In turn they can guide history taking.
Health-related quality of life (HRQoL)
HRQoL refers to the physical, psychological and social domains of health unique to the
individual101. Domains generally excluded from HRQoL are income, freedom and
environment102. Tools to measure HRQoL are commonly used in research in chronic or terminal
96
OECD. Measuring Social Well-being. Paris 1976
Najman JM, Levine S. Evaluating the impact of medical care and technologies on the quality of life: a
review and critique. Soc Sci & Med 1981; 15F:107-115
98
Jones PW. Health status measurement in chronic obstructive pulmonary disease. Thorax 2001; 56:880887
99
Sen K, Bonita R. Global health status: two steps forward, one step back. Lancet 2000; 356:577-582
100
Murray CJL. Quantifying the burden of disease: the technical basis for disability adjusted life years. In:
Murray CJL, Lopez AD, eds. Global Comparative Assessments in the Health Sector. Geneva: WHO, 1994.
pp3-16,
101
Testa MA, Simonson DC. Assessment of quality-of-life outcomes. New Engl J Med 1996; 334:835-840
102
Guyatt GH, Feeny DH, Patrick DL. Measuring health-related quality of life. Ann Intern Med 1993;
118:622-629
97
26
disease, but their application to routine clinical practice is small. Early instruments to measure
HRQoL, particularly in cancer research, were uni-dimensional103, but more recent models in
chronic diseases have been multi-compartmental. Social and cultural contexts, physical and
psychological illness, the amount of perceived freedom, achievement of ambitions, the matching
of achievements to expectations, all impact on HRQoL.
The level of HRQoL in people with chronic illness is independently associated with risk of
unplanned readmission to hospital104, and with higher rates of depression105,106. In chronic
diseases like COPD, HRQoL measures aim to quantify the well-being of an individual and
catalogue the contributing factors. The tools can be adapted for use in clinical care107.
Disease-specific measures
These tools reflect the impact of a specific condition or organ-related abnormality on the
individual. In general, they are more sensitive to change. Effects of an intervention on dimensions
that are not included, however, may be missed in these more specific tools. In a recent UK study,
disease-specific health status was worse in people with COPD than in an age-matched reference
population108, and declined progressively.
Generic measures
Generic tools allow us to compare the overall HRQoL of different chronic health conditions.
They need to include a wide range of dimensions, which means their utility and responsiveness to
change may be sacrificed because they need to be extensive or else their dimensions are
addressed with such brevity. In the UK study referred to above, generic health status in people
with COPD was barely different from age-matched controls109, although a linear deterioration in
generic health status over three years was demonstrated in those with COPD.
Disease-specific and generic measures have both recently been found in COPD to be related to
health-care utilisation110, and capable of predicting survival111, and this inter-relationship becomes
more significant in older individuals, those have higher levels of depression and those who are
more symptomatic, regardless of gender112. The possibility exists that the relationship between
103
Karnovsky D, Burchenal J. The clinical evaluation of chemotherapeutic agents in cancer. In: Macleod C,
ed. Evaluation of chemotherapeutic agents. NY: Columbia University Press, 1949. pp191-205
104
Pearson S, Stewart S, Rubenach S. Is health-related quality of life among older, chronically ill patients
associated with unplanned readmission to hospital? Aust NZ J Med 1999; 29:701-706
105
Bosley CM, Corden ZM, Rees PJ, Cochrane GM. Psychological factors associated with the use of home
nebulized therapy for COPD. Eur Respir J 1996; 9:2346-2350
106
Cleland JA, Lee AJ, Hall S. Associations of depression and anxiety with gender, age, health-related
quality of life and symptoms in primary care COPD patients. Family Practice 2007; 24:217-223
107
Higginson IJ, Carr AJ. Using quality of life measures in the clinical setting. Brit Med J 2001; 322:12971300
108
Spencer S, Calverley PMA, Burge PS, Jones PW. Health status deterioration in patients with chronic
obstructive pulmonary disease. Am J Respir Crit Care Med 2001; 163:122-128
109
Spencer S, Calverley PMA, Burge PS, Jones PW. ibid
110
Desikan R, Mason HL, Rupp MT, Skehan M. Health-related quality of life and health care resource
utilisation by COPD patients: a comparison of three instruments. Qual Life Res 2002; 11:739-751
111
Domingo-Salvany A, Lamarca R, Ferrer M, Garcia-Aymerich J, et al. Health-related quality of life and
mortality in male patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2002;
166:680-685
112
Budweiser S, Hitzl AP, Joerres RA, et al. Health-related quality of life and long-term prognosis in
chronic hypercapnic respiratory failure: a prospective survival analysis. Respir Research 2007; 8:92
27
health care utilization and HRQOL may be in either direction113. HRQoL may therefore provide a
basis for staging COPD in functional terms114,115 to supplement lung function staging, as the two
116,117,118
, and HRQoL may better
indicators may reflect different patient or disease characteristics
capture the systemic effects of COPD119.
113
Garrido PC, Diez JdeM, Gutierrez JR, et al. Negative impact of chronic obstructive pulmonary disease
on the health-related quality of life of patients. Results of the EPIDEPOC study. Health Qual Life
Outcomes 2006; 4:31-39
114
Stahl E, Lindberg A, Jansson S-A, Ronmark E, et al. Health-related quality of life is related to COPD
severity. Health Qual Life Outcomes 2005; 3:56
115
Hajiro T, Nishimure K, Tsukino M, et al. A comparison of the level of dyspnoea vs disease severity in
indicating the health-related quality of life of patients with COPD. Chest 1999; 116:1632-1637
116
Hajiro T, Nishimure K, Tsukino M, et al. ibid
117
Tsukino M, Nishimura K, Ikeda A, Koyama H, et al. Physiologic factors that determine the healthrelated quality of life in patients with COPD. Chest 1996; 110:896-903
118
Mahler DA, Mackowiak JI. Evaluation of the short-form 36-item questionnaire to measure healthrelated quality of life in patients with COPD. Chest 1995; 107:1585-1589
119
van Manen JG, Bindelo PJ, Dekker FW, Bottema BJ, et al. The influence of COPD on health-related
quality of life independent of the influence of comorbidity. J Clin Epidemiol 2003; 56:1177-1184
28
QUALITY OF LIFE
KEY POINTS
1)
Quality of life refers to an individual’s happiness.
2)
Health status reflects the well-being of groups
3)
Health-related quality of life can be measured with generic or
disease-specific tools
4)
Generic tools enable comparisons between different disease
groups
5)
Disease-specific tools are sensitive to respiratory disability
and handicap, and sensitive to change
INDICATORS
KEY POINTS
1)
Clinical indicator assessment should include impairments,
disability, handicap and costs
2)
Spirometry, lung volumes, and gas transfer reflect respiratory
impairments
3)
Exercise tests reflect respiratory impairment and disability
4)
Psychological impairments include stable personality traits, mood
states, emotions
5)
Nutritional status is an independent prognostic indicator
6)
Disability and handicap can be quantitated using quality of life
measures
2.3 Disease Management
The philosophy of management of chronic complex diseases should incorporate patient-focussed
evidence-based care through the disease continuum. �Chronic Disease Management’ (CDM) has
emerged as a systematic approach to managing all aspects of a disease, from primary prevention,
29
through provision of cost-effective combinations of interventions aimed at optimising disease
control, improving lifestyle factors influencing the disease, right to the end of life. It encourages
holistic patient-centred care of people with chronic conditions and their family/informal
caregivers within a care partnership, monitoring and constantly improving processes and clinical
outcomes of interventions so that efficacy, effectiveness and cost-effectiveness are optimised.
Most chronic respiratory conditions have a progressive natural history that commences with
minimal symptoms and mild impairment, and progresses to a systemic condition with severe
handicap. Symptoms are generic – breathlessness with exertion, cough, and sputum production –
and concurrent morbidities are common. These may be systemic manifestations of underlying
inflammation, organ-based complications that result from the physiological or psychological
stresses created by the severity of underlying disease, or in some cases adverse effects of
treatments. Some may be present because they share either aetiology (smoking, pollution, etc) or
age-related organ degeneration. All need attention in treating the respiratory disease.
Systemic manifestations of COPD include
• cor pulmonale and right heart failure
• polycythaemia
• loss of cardiovascular conditioning
• poor nutrition
• muscle weakness
• cognitive impairment
• mood disturbances
Adverse effects of treatment include
• osteoporosis, cataracts, proximal myopathy, systemic hypertension, psychoses, insomnia,
peptic ulceration and diabetes associated with oral corticosteroids
• glaucoma and bladder outlet obstruction with anticholinergics
• cardiac arrhythmias and tremor with beta-receptor agonists or theophylline
• gastro-oesophageal reflux, peptic ulceration, nausea and seizures with theophylline
• candidiasis, skin fragility and bruising, and dysphonia from inhaled corticosteroids.
Conditions that share aetiology or are age-related include
coronary artery disease
cerebrovascular disease
peripheral vascular disease
lung and other cancers
obstructive sleep apnoea (with obesity, hypertension, hypogonadism, etc)
diabetes mellitus
Consequences of the burden of disablement are largely psychological and social:
• depression
• panic/anxiety
• social isolation
• dependency on spouses and family
• carer burden
A holistic approach to management of chronic complex respiratory conditions is likely to provide
best outcomes. Providers of care should have expertise to identify and treat the concurrent
morbidities, and support systems should cover the range of impairments, disabilities and
30
handicaps both of the primary disease and the concurrent conditions. CDM must encourage
primary prevention and earlier detection of diseases, more equitable distribution of treatments,
and better care for people with later stages of chronic complex diseases. It should give guidance
for managing the continuously evolving nature of the conditions. Systems that support integrated
self-management should aim to maintain better health for longer at the community level and
reduce the need for crisis care. Integral to disease management in advanced respiratory disease
are treatments for dyspnoea, palliative approaches, planning advanced directives and linking
hospital management to community care guidelines.
Respiratory health professionals should be partners in initiatives that apply to the care continuum.
Primary and secondary prevention involvement includes lifestyle, nutrition and quit-smoking
projects (eg in schools, in general practice and in hospitals), and better identification of smokers
at all ages. Providers (GPs, nurses and hospital doctors) should be trained to encourage behaviour
change that leads to sustained quitting.
2.4 Impairment, Disability and Handicap
The World Health Organization (WHO) developed definitions in 1980120 that provided distinct
albeit inter-related consequences of disease.
Impairment refers to an injury or abnormality occurring at the individual or
organ system level representing “any loss or abnormality of psychological,
physiological, or anatomic structure or function”. Measurement of impairment
typically focuses on severity of a deficit existing in the organ or system of
interest, and usually requires disease- or organ-specific tools.
Disability may arise from an impairment or combination of impairments or
diseases. Disability is primarily a social construct that occurs at the person level,
and represents “any restriction or lack (resulting from an impairment of ability
to perform an activity in the manner or within the range considered normal for a
human being”. Measurement of a disability is typically generic, and assesses the
degree of independence with which an individual can perform activities of daily
living.
Handicap arises from disabilities and impairments, and is the “disadvantage for
a given individual that limits or prevents the fulfilment of a role that is normal
(depending upon age, sex, social and cultural factors) for that individual”.
Measurements of handicap address social roles, independence, mobility, social
integration, productivity and economic self-sufficiency.
More recently the WHO has attempted to provide a classification of functioning and disability.
that covers any disturbance in terms of “functional states” associated with health conditions,
organized according to three dimensions – body level, individual and society levels121. It
120
World Health Oganization. WHO international classification of impairments, disabilities and handicaps:
a manual of classification relating to the consequences of diseases. Geneva: World Health Organization
1980
121
World Health Organization. International classification of functioning, disability and health.
http://www3.who.int/icf/
31
addresses body functions, activities and social participation, treating all diseases on an equal
footing for equitable comparison and combining them into a functionality framework.
2.5 Outreach and Home Care
The concept of providing care for people away from hospital is based on a desire to continue care
for the aged and infirm at home for as long as possible. Hospitals and Community Health Centres
have for many years employed health workers to provide community care and support. People
prefer to avoid hospital care if they can, contagious diseases are issues in hospitals, and hospital
funding is increasingly expensive and rationed. Visiting patients at home is a positive experience
for patients, carers and health workers. It gives health workers a better insight into the difficulties
patients and their carers have at home, provides patients and carers more confidence that the
home environment is appropriate, and assists with personalising equipment and care needs.
Common examples of home-based and outreach care include wound care post-surgery, diabetes
education and care, home-based rehabilitation after stroke or musculoskeletal surgery, and
cardiac care post-myocardial infarction. In the field of respiratory diseases Respiratory Nurses
from teaching hospitals typically visit patients with severe COPD or people with home oxygen to
monitor progress or provide education about ongoing management. Nurses from Chest or TB
Clinics screen and monitor contacts of people with tuberculosis. Hospital-At-Home professionals
provide treatment of illnesses like pneumonia or post-operative wound care. Domiciliary Care or
District Nursing Services workers (such as occupational therapists, nurses, physiotherapists,
podiatrists, and carers) can provide health care services at home. GP surgeries are increasingly
utilising specialist Practice Nurses to help people with COPD, diabetes, asthma and other
conditions to understand their condition and its most effective management.
There is a paucity of strong evidence supporting use of home care for people with chronic
respiratory diseases. A recent American Thoracic Society Statement pointed to the complexities
of home care that need to be accounted for in determining costs and effectiveness122, and few of
its recommendations had significant evidence base. This will be reviewed later in the Manual.
2.6 Pulmonary Rehabilitation (PR)
The definition of PR has undergone several evolutions since the development of the first
programs in USA in the 1970's. Definitions from US professional bodies include:
"Pulmonary rehabilitation is a multi-dimensional continuum of services directed to
persons with pulmonary disease and their families, usually by an interdisciplinary
team of specialists, with the goal of achieving and maintaining the individual's
maximum level of independence and functioning within the community."123
"Pulmonary rehabilitation may be defined as an art of medical practice wherein an
individually tailored, multidisciplinary program is formulated which through
122
Narsavage GL, et al, for ATS Board of Directors. Statement on Home Care for patients with Respiratory
Disorders. Am J Respir Crit Care Med 2005; 171:1443-1464
123
Fishman AP. NIH Workshop summary. Pulmonary rehabilitation research. Am J Respir Crit Care Med
1994; 149:825-833
32
accurate diagnosis, therapy, emotional support, and education, stabilizes or
reverses both the physio- and psychopathology of pulmonary diseases and attempts
to return the patients to the highest possible functional capacity allowed by his
pulmonary handicap and overall life situation."124
British125 and European126,127 guidelines reflect these definitions. The most recent Statement on
PR from the American College of Chest Physicians (ACCP), the American Association of
Cardiovascular and Pulmonary Rehabilitation (AACVPR), the American Thoracic Society (ATS)
and European Respiratory Society (ERS) define PR as:
“..an evidence-based, multi-disciplinary, and comprehensive intervention for
patients with chronic respiratory diseases who are symptomatic and often have
decreased daily life activities. Integrated into the individualized treatment of the
patient, pulmonary rehabilitation is designed to reduce symptoms, optimize
functional status, increase participation, and reduce health care costs through
stabilizing or reversing systemic manifestations of the disease.” 128.129
The concept emphasises that practitioners of PR should have in mind a multidisciplinary
approach to overall disease management that addresses physical and social function of the
individual and give attention to early detection and both primary and secondary prevention.
Numerically by far the greatest experience in PR is for patients with COPD, though people with a
very wide range of respiratory conditions actually attend programs. This Manual concentrates on
COPD, with additional comments about other conditions where evidence exists, or where logic
and consensus suggest either benefit or contraindications exist. The components of PR are
detailed in the text.
The primary aim of pulmonary rehabilitation then is to reduce disability and handicap of persons
with chronic lung diseases and support their carers, thereby restoring the patient to the highest
possible level of independent functioning. It should be part of the integrated lifetime management
of people with chronic respiratory disease.
2.7 Self-Management for Chronic Disease
Traditional approaches to medical care have arisen from the need to "cure" acute disease. Greater
longevity and the trend to unhealthy lifestyle habits in the past 100 years have contributed to the
emergence of chronic degenerative diseases, for which "cure" is rarely possible, and acute care
approaches are ineffective. Indeed, 30 years ago around 80% of US health resources were already
124
AACVPR/ACCP Pulmonary Rehabilitation Guidelines Panel. Pulmonary Rehabilitation. Joint
ACCP/AACVPR evidence-based guidelines. Chest 1997; 112:1363-1396
125
British Thoracic Society Standards of Care Subcommittee on Pulmonary Rehabilitation. Pulmonary
rehabilitation. Thorax 2001; 56:827-834
126
Donner CF, Muir JF. Selection criteria and programmes for pulmonary rehabilitation in COPD patients.
Eur Respir J 1997; 10:744-757
127
Donner CF, Decramer M. Pulmonary rehabilitation. Eur Resp Soc Monogr 2000; 13
128
Nici L, Donner C, Wouters E, et al. American Thoracic Society/European Respiratory Society Statement
on Pulmonary Rehabilitation. Am J Respir Crit Care Med 2006; 173:1390-1396
129
Ries AL, Bauldhoff GS, Carlin BW, Casaburi R, et al. Pulmonary rehabilitation: Joint ACCP/AACVPR
evidence-based clinical practice guidelines. Chest 2007; 131:4-42
33
expended on the care of people with chronic conditions130. Increasing longevity is further adding
to the prevalence and burden of such conditions.
Patients with chronic health conditions experience variations in symptoms, which often result in
disruptive and expensive hospitalisation. Yet they ought to be ideally placed to monitor and
manage their own symptoms. A team approach to care that trades off this capacity of the patient
and their doctor's scientific knowledge to interpret and respond to changes in symptoms offers
scope for individualised rapid-response care. This requires adequate training for patients to
respond with appropriate interventions under the guidance of medically agreed pathways131.
Self-management refers to people with chronic diseases "engaging in activities that protect and
promote health, monitoring and managing…symptoms and signs of illness, managing the impacts
of illness on functioning and interpersonal relationships and adhering to treatment regimes"132.
This approach requires health care providers and health care systems to support the central role of
patients in managing their own chronic illness, and there is mounting evidence for its
effectiveness133. Perhaps the term “co-management” would be more applicable..
Again, as with home care, evidence relating to self-management approaches for people with
chronic respiratory disease is lacking. This will be reviewed later in the Manual.
2.8 Support Groups
Support Groups (SG) for chronic lung disease aim to empower patients to take a more active role
in their own health management and enable them to take charge of the physical and psychosocial
impacts of their disease. They help patients and carers find enjoyment in a renewed quality of life
through information, education, friendship, encouragement and shared experiences, and reduced
social isolation.
The ALF has facilitated the development of over 120 groups around Australia, with over 11,000
members around the nation under the banner of LungNet. The LungNet encourages independence
and self-motivation of groups, and advises them to meet regularly, have guest speakers with a
range of interesting topics related to the health condition and its management, and address social
issues. Member-to-member support, transport assistance, social outings and telephone contact,
especially for the carer at times of hospitalisation, appear useful.
The benefits of SGs to people with COPD are as yet unproven, however. They have a
demonstrable role in other chronic conditions, and it seems likely that similar benefits could be
shown in chronic lung disease. It has been claimed that SGs facilitate the rehabilitation of people
with COPD134, and it has been included as an arm in disease management of COPD135, despite the
130
Cluff L. Chronic disease, function and quality care. J Chronic Disability 1981; 34:299-304
Wagner EH. The role of patient care teams in chronic disease management. Brit Med J 2000; 320:569572
132
Lorig K. Self-management of chronic illness: A model for tertiary prevention (Perspectives on chronic
illness: Treating patients and delivering care). Am Behav Scientist 1993; 39:676-678
133
Lorig KR, Sobel DS, Stewart AL, Brown BW, et al. Evidence suggesting that a chronic disease selfmanagement program can improve health status while reducing hospitalisation: a randomised trial. Medical
Care 1999; 37:5-14
134
Burns M. Continuing care programs. In: Principles and Practice of Pulmonary Rehabilitation. Eds R
Casaburi and TL Petty. Philadelphia: WB Saunders: pp398-404, 1993
131
34
absence of substantiating data. Since the effects of a specific PR program package wane if
exercise, education and psychosocial support are not maintained, SGs have the potential to
promote continuation of activities and information.
135
Tiep BL. Disease management of COPD with pulmonary rehabilitation. Chest 1997; 112:1630-1656
35
3. EPIDEMIOLOGY AND BURDEN
OF CHRONIC LUNG DISEASE
COPD is one of the five most important causes of death and disability world-wide. In white males
living in developed nations the increasing prevalence and mortality have been slowing in recent
years (unlike cardiovascular diseases, where rates have been declining). Rates in the developing
world, and in women as well as black males in developed nations, continue to increase136.
3.1 Prevalence and Incidence
The Australian Institute of Health and Welfare (AIHW) reported almost 300,000 Australians with
COPD in 1996 (prevalence), with more than 20,000 new cases being diagnosed every year
(incidence)137. A population based assessment model used by the WHO has been applied to the
Australian population characteristics and estimates 558,000138 people with moderate to severe
COPD in the year 2000. The true incidence, prevalence, morbidity and mortality of COPD in
Australia are uncertain, however. The Australian Institute for Health and Welfare (AIHW) admits
recent estimates probably under-represent the magnitude of the problem139. Prevalence estimates
from a general population in Melbourne suggest 12% of people aged 45-69 years had
symptomatic COPD140. Results from the Burden of Obstructive Lung Disease (BOLD) are also
pointing to rates of symptomatic disease around 10-12%141.
The benchmark for diagnosis of COPD is spirometry, as it identifies airflow limitation, the major
diagnostic criterion. Obtaining reliable prevalence data for COPD is complicated by how the
condition is labelled (since chronic bronchitis, emphysema or COPD are coded differently).
Prevalence can be based on patient self-report of symptoms, or by examining administrative
databases (such as specified prescriptions in certain age-groups, or death records, or established
diagnosis by doctors, or on presence of airflow limitation. Self-report provides an estimate
(albeit poorly validated) of all Stages of symptomatic disease (including those at-risk), with
prevalence rates reported at up to 24% in smokers and 6.5% in ex-smokers142. COPD, however, is
136
Bailey WC, Ferguson GT, Higgins M, et al for The National Lung Health Education Program Executive
Committee. Strategies in preserving lung health and preventing COPD and associated diseases. The
National Lung Health Education Program (NLHEP). Chest 1998; 113(Suppl):123S-163S
137
Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. AIHW cat. no. PHE 17.
Canberra: AIHW; 1999
138
Tan WC, Seale P, Chaoenrantanakul S, Hardiarto M, et al. Chronic obstructive pulmonary disease
(COPD) prevalence in 7 Asian countries: Projections based on the COPD Prevalence Model. Am J Respir
Crit Care Med 2001; 163 (Suppl):A81
139
Australian Institute of Health and Welfare. Australia’s Health 2006; the tenth report of the Australian
Institute of Health and Welfare. Ed P Magnus. AIHW cat. No. AUS73. Canberra: AIHW: pages 83-87
140
Abramson M, Matheson M, Wharton C, et al. Prevalence of respiratory symptoms related to chronic
obstructive pulmonary disease and asthma among middle-aged and older adults. Respirology 2002; 7:325331
141
Buist AS, McBurnie MA, Vollmer WM, Gillespie S, et al. International variation in the prevalence of
COPD (The BOLD Study): a population-based prevalence study. Lancet 2007; 370:741-750
142
National Center for Health Statistics. Current estimates from the National Health Interview Survey,
United States, 1995. Washington, DC: Department of Health and Human Services, Public Health Service,
Vital and Health Statistics. Publication Number 96-1527; 1995
36
usually not recognised and diagnosed until it is moderately advanced with significant impact on a
person’s lifestyle143,144,145.
Doctor diagnosis is better validated for estimates of symptomatic and disabling COPD, and has
been found in 6.4% of the UK population based on general practitioner databases146. This study
also found that doctor-diagnosed COPD had increased gradually over 1990 to 1997 in women at
all ages (overall increase 68%), with a plateau in prevalence in men. Prevalence, hospitalisation
and mortality all increased markedly with age beyond 40 years in both men and women, and
prevalence rates over age 65 were similar between the sexes. However, such diagnoses are
infrequently based on objective findings from spirometry, and data using this approach can underestimate the prevalence. For example, providing open access to spirometry in a primary care area
in UK was reported to have discovered 91 previously undiagnosed cases of COPD in 217 patients
with complete records and spirometry results (42% rate of non-diagnosis)147.
Examination of GP databases in the group referred to above (representing around 10% of the
England and Wales population) has since been carefully validated as an indicator of both disease
incidence and prevalence148. An alternative administrative database has been used in Italy,
consisting of repeated drug prescriptions of respiratory drugs, antibiotics and oral
corticosteroids149. In the latter, the overall adult population prevalence of COPD was 3.6%.
Mortality rates have also been used to determine disease prevalence, but attribution on death
certificates to COPD as the primary cause of death (and often even as a contributory factor) has
often been found deficient150. Nevertheless, mortality rates for COPD have shown similar rising
trends, faster in women than in men, and equalization of mortality rates in men and women151.
The objective measurement of airflow limitation in random population surveys shows
prevalence rates of 14.2% in male current smokers and 13.6% in female current smokers, but
3.3% in never-smoking males and 3.1% in never-smoking females152 in USA. In UK
opportunistic screening at the primary care level showed prevalence rates of 9%153. A more
143
Draft Executive Summary, Global Strategy for the Diagnosis, Management and Prevention of Chronic
Obstructive Pulmonary Disease. NHLBI, WHO, September 2000
144
Wilson DH, Tucker G, Frith P, et al. Trends in hospital admissions and mortaltity from asthma and
chronic obstructive pulmonary disease in Australia, 1993-2003. Med J Aust 2007; 186:408-411
145
Rabe KF, Hurd S, Anzueto A, et al. Global Strategy for the diagnosis, management, and prevention of
COPD: GOLD executive summary. Am J Respir Crit Care Med 2007; 176:532-555
146
Soriano JR, Maier WC, Egger P, Visick G, et al. Recent trends in physician diagnosed COPD in women
and men in the UK. Thorax 2000; 55:789-794
147
Walker PP, Mitchell P, Diamantea F, et al. Effect of primary-care spirometry on the diagnosis and
management of COPD. Eur Respir J 2006; 28:945-952
148
Soriano JR, Maier WC, Visick G, Pride NB. Validation of general practitioner-diagnosed COPD in the
UK General Practice Database. Eur J Epidemiol 2001; 17:1075-1080
149
Anecchino C, Rossi E, Fanizza C, De Rosa M, et al. Prevalence of chronic obstructive pulmonary
disease and patterns of comorbidities in a general population. Int J COPD 2007; 2:567-574
150
Sherrill DL, Lebowitz MD, Burrows B. Epidemiology of chronic obstructive pulmonary disease. Clin
Chest Med 1990; 11:375-387
151
Mannino DM, Homa DM, Akinbami LJ, et al. Chronic obstructive pulmonary disease surveillance:
United States, 1971-2000. MMWR Morb Mortality Wkly Rep 2002; 51:1-16
152
National Center for Health Statistics. Current estimates from the National Health Interview Survey,
United States, 1995. Washington, DC: Department of Health and Human Services, Public Health Service,
Vital and Health Statistics. Publication Number 96-1527; 1995
153
Seamark DA, Williams S, Timon S, et al. Home or surgery based screening for chronic obstructive
pulmonary disease (COPD)? Prim Care Resp J 2001; 10:30-33
37
comprehensive screening was conducted among 22 GPs in Belgium over twelve weeks and
uncovered new COPD in 18% of the symptomatic population and 4% of the asymptomatic
patients154. It has proven possible to screen high-risk populations using spirometry, such as the
�Know The Age Of Your Lungs Project’ in Poland, where 110,355 people were tested over three
years155. Respiratory symptoms were reported by over half, and airflow limitation was found in
20.3%, more commonly in smokers and in rising numbers with increasing age. A random sample
of 1,500 northern Swedish people from an earlier cohort of 6,610 was surveyed with interviews
and lung function tests. COPD (airflow limitation post-bronchodilator) was diagnosed in 14.3%,
increasing in older groups, and higher in those with greatest lifetime cigarette exposure, but only
half had been previously diagnosed156. A study conducted in Israel in 20 pack-year current and
former smokers aged 45 and over (n=1,150) evaluated symptoms and spirometry abnormalities.
Airflow limitation was found in 22%, and most had moderate stage COPD157 (with only 4%
having a previous diagnosis of COPD). Based on such findings it is reasonable for the GOLD
Workshop to have concluded that available prevalence and morbidity data are likely to
underestimate the total burden of disease158.
In a combined self-report and lung function study reported in 1996 from the UK, a respiratory
symptoms questionnaire was sent to people over age 45 randomly selected from general
practitioner patient lists. There was a high response rate of 92.3%159, making the results reliable.
Of the 723 subjects, 29.2% were smokers and 37.3% were ex-smokers. Respiratory symptoms
were reported by 30.0%, of whom almost half were using inhaled medications. Of the responders
to a full questionnaire 62.5% attended for lung function testing, and in 26.4% of these airflow
limitation was identified. Only half the people with airflow limitation and respiratory symptoms
had been diagnosed with respiratory disease by a doctor, so there was significant underdiagnosis,
as well as misclassification as other conditions like asthma. A recent survey with a similar model
conducted in general practices in Australia revealed similar findings160, and this has been
confirmed in a general population survey conducted prior to release of COPD-X161. In adults aged
45-70 years, 3.5% had COPD and 3.6% had mixed asthma and COPD162. Over 40% did not have
a prior diagnosis of COPD, and almost half had received no prescribed respiratory medications.
154
Buffels J, Degryse J, Heyrman J, Decramer M. Office spirometry significantly improves early detection
of COPD in general practice: the DIDASCO Study. Chest 2004; 125:1394-1399
155
Zielinski J, Bednarek M, Gorecka D. In �The Global Burden of Chronic Obstructive Pulmonary Disease;
Increasing COPD awareness’. Eds KF Rabe, JB Soriano. Eur Respir J 2006; 27:833-852
156
Lindberg A, Bjerg-Backlund A, Ronmark E, et al. Prevalence and underdiagnosis of COPD by disease
severity and the attributable fraction of smoking: Report from the Obstructive Lung Disease in Northern
Swedish Studies. Respir Med 2006; 100:264-272
157
Stav D, Raz, Meir. Prevalence of chronic obstructive pulmonary disease among smokers aged 45 and up
in Israel. IMAJ 2007; 9:800-802
158
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
159
Renwick DS, Connolly MJ. Prevalence and treatment of chronic airways obstruction in adults over the
age of 45. Thorax 1996; 51:164-168
160
Frith P, Esterman A, Crockett A, McKenzie D. Audit of COPD diagnosis and management in a primary
care setting. Australian Lung Foundation 2004
161
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
162
Matheson MC, Abeysena C, Raven JM, et al. How have we been managing chronic obstructive
pulmonary disease in Australia? Intern Med J 2006; 36:92-99
38
The ALF commissioned a review of data from the AIHW and New Zealand (NZ) Ministry of
Health163; an update is expected in late 2008. COPD is the third leading cause of �burden of
disease’ in Australia164 behind Ischaemic Heart Disease and Stroke. COPD is the largest
contributor to the burden of disease associated with all respiratory conditions (including asthma),
three times the burden of acute respiratory infections and more than four times the burden of
other chronic respiratory diseases165. The burden of COPD is escalating worldwide. The 1996
Global Burden of Disease Study compared the leading causes of disability in 1990 and 2020
(projected). In 1990 COPD was globally ranked 12th, but it is projected to rank 5th in 2020, behind
ischaemic heart disease, major depression, traffic accidents and cerebrovascular disease166. A
meta-analysis of studies evaluating population prevalence published in 2006167 included research
reports that documented (a) total population or sex-specific estimates for COPD, Chronic
Bronchitis and / or emphysema, and (b) detailed information on diagnostic criteria used. Of 5,464
articles screened 356 met inclusion criteria, and 67 articles were subjected to meta-analysis. Data
were available for 28 countries. Spirometric-diagnosed COPD (26 estimates) provided a pooled
prevalence of 9.2% (95% CI=7.7-11.0), while doctor-diagnosis gave pooled prevalence rates of
5.2% for COPD and 5.3% for Chronic Bronchitis.
Given the deficiencies in methodologies and data up to 2006, the Burden of Obstructive Lung
Disease (BOLD) survey findings are keenly awaited. This global survey, being conducted in
representative populations with questionnaire and lung function measures, should provide
comprehensive data about COPD prevalence and burden. The current analyses suggest that adult
population prevalence rates are in the range from 10 to 15%168.
Incidence of COPD is more difficult to document, as it relies on prospectively-collected data and
accurate diagnosis. The European Community Respiratory Health Survey (ECRHS) began in
1991-1993 to examine a random sample of 14,252 young adults aged 20-44169, with follow-up in
1999-2002170. Valid lung function measurements were obtained in 5,002 of the 9,839 eligible
subjects without initial airflow obstruction or asthma, and demonstrated an annual incidence of
COPD of 2.8 cases/1,000/year (95% CI=2.3-3.3)171; the 10-year cumulative incidence of GOLD
Stage II in male smokers in their fifties was around 25%. In a smaller northern Swedish study, the
163
Crockett AJ, Cranston JM, Moss JR. Economic Case Statement. Chronic obstructive pulmonary disease
(COPD). The Australian Lung Foundation; 2002
164
Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia. AIHW cat. no. PHE 17.
Canberra: AIHW; 1999
165
Australian Institute of Health and Welfare. Australia’s Health 2000: the seventh biennial health report of
the Australian Institute of Health and Welfare. Canberra: AIHW; 2000
166
Murray CJL, Lopez AD, Eds. The global burden of disease: a comprehensive assessment of mortality
and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Cambridge, MA:
Harvard University Press; 1996.
167
Halbert RJ, Natoli JL, Gano A, et al. Global burden of COPD: systematic review and meta-analysis. Eur
Respir J 2006; 28:523-532
168
Buist AS, McBurnie MA, Vollmer WM, et al. International variation in the prevalence of COPD (The
BOLD Study): a population-based prevalence study. Lancet 2007; 370:741-750
169
Burney PC, Luczynska, Chinn S, Jarvis D. The European Community Respiratory Health Survey. Eur
Respir J 2005; 26(Suppl 49):434S.
170
European Community Respiratory Health Survey II Steering Committee. The European Community
Respiratory Health Survey II. Eur Respir J 2002; 20:1071-1079.
171
deMarco R, Accordini S, Cerveri I, Corsico A, et al. Incidence of chronic obstructive pulmonary disease
in a cohort of young adults according to the presence of chronic cough and phlegm. Am J Respir Crit Care
Med 2007; 175:32-39
39
cumulative 10-year incidence was 13.5% in a symptomatic cohort172. A Finnish study of 40-64
year old male smokers found an annual incidence of 0.5%173. Polish male smokers aged 41-60
had a mean annual incidence of COPD with FEV1 < 65% predicted of 1.2-1.6%174. In a general
practice setting in Netherlands, all males aged 40 to 65 years were screened, those without known
lung disease were invited for spirometry, and those with normal initial spirometry or GOLD
Stage I COPD were followed up with spirometry after another five years. The 5-year cumulative
incidence of GOLD Stage II COPD was 8.3% (mean 1.6% per annum)175.
3.2 Risk factors for COPD
Smoking is the major risk factor for developing COPD, though current understanding of risk cofactors is incomplete. Risk factors fall into two categories - host factors and environmental
exposures. Some are known to cause COPD, while others, in combination, may increase an
individual's risk and speed progression of COPD. One of the best-know host factors (Table 3.1) is
the genetic linkage of deficiency of alpha-1-antrypsin (or antiproteinase)176. The multi-centre
randomized clinical trial comparing lung volume reduction surgery with medical management for
severe COPD, the National Emphysema Treatment Trial (NETT), has identified polymorphisms
in a range of genes associated with airflow abnormalities177, and other COPD phenotypes and
characteristics178. A family history of respiratory disease may be an independent risk factor,
although this is hard to separate from parental smoking.
172
Lingbergh A, Jonsson A-C, Ronmark E, et al. Ten-year cumulative incidence of COPD and risk factors
for incident disease in a symptomatic cohort. Chest 2005; 127:1544-1552
173
Huhti E, Ikkala J. A follow-up study on respiratory symptoms and ventilatory function in a middle-aged
rural population. Eur I Respir Dis 1980; 61:33-45
174
Krzyzanowski M, Jedrychowski W, Wysocki M. Factors associated with the change in ventilatory
function and the development of chronic obstructive pulmonary disease in a 13-year follow-up of the
Cracow Study: Risk of chronic obstructive pulmonary disease. Am Rev Respir Dis 1986: 134:1011-1019
175
Geijer RMM, Sachs APE, Verheij TJM, Salome PL, Lammers J-WJ, Hoes AW. Incidence and
determinants of moderate COPD (GOLD II) in male smokers aged 40-65 years: 5-year follow up. Brit J
Gen Pract 2006; 56:656-661
176
Hubbard RC, Crystal RG. Antiproteinases. In: Crystal RG, West JB, Barnes PJ, Cherniak NS, Weibel
ER, eds. The Lung: Scientific Foundations. New York: Raven Press Ltd: 1991. pp1775-1787
177
DeMeo DL, Celedon JC, Lange C, Reilly JJ, et al. Genome-wide linkage of forced mid-expiratory flow
in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2004; 170:1294-1301
178
Hersh CP, DeMeo DL, Lazarus R, Celedon JC, et al. Genetic association analysis of functional
impairment in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2006; 173:977-984
40
TABLE 3.1. HOST-RELATED RISK FACTORS FOR COPD179,180
Host
Factors
Factor
Age
Gender
Race/Ethnicity
Genes (e.g. deficiency of alpha-1-antitrypsin)
Asthma
Airway hyper-responsiveness
Familial (?genetic) clustering
Lung growth
Relationship & level of evidence
Causal (II)181,182
Additive (III)183
Additive (III)184,185
Causal (II)186
Causal (II)187,188,189 or Additive (II)190,191
Additive (III)192,193
Additive (II)194,195
Causal (IV)196,197
179
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
180
Rabe KF, Hurd S, Anzueto A, et al. Global Strategy for the diagnosis, management, and prevention of
COPD: GOLD executive summary. Am J Respir Crit Care Med 2007; 176:532-555
181
Higgins MW, Keller JB, Becker M, et al. An index of risk for obstructive airways disease. Am Rev.
Respir Dis. 1982; 125:144-151
182
Sherrill DL, Lebowitz MD, Burrows B. Epidemiology of chronic obstructive pulmonary disease. Clin
Chest Med 1990;11:375-387
183
Prescott E, Bjerg AM, Andersen PK, et al. Gender difference in smoking effects on lung function and
risk of hospitalization for COPD: results from a Danish longitudinal population study. Eur Respir J
1997;10:822-7
184
Horne SL, Cockcroft DW. Ethnicity as a possible factor contributing to the development of chronic
airflow limitation and asthma. Clin Invest Med 1990; 13:333-338
185
Samet JM, Coultas DB, Howard CA, Skipper BJ. Respiratory disease and cigarette smoking in a
Hispanic population in New Mexico. Am Rev Respir Dis 1988; 137:815-9
186
Hubbard RC, Crystal RG. Antiproteinases. In: Crystal RG, West JB, Barnes PJ, Cherniak NS, Weibel
ER, eds. The Lung: Scientific Foundations. New York: Raven Press Ltd: 1991. pp1775-1787
187
Brown PJ, Greville HW, Finucane KE. Asthma and irreversible airflow obstruction. Thorax 1984;
39:131-136
188
Silva GE, Sherrill DL, Guerra S, Barbee RA. Asthma as a risk factor for COPD in a longitudinal study.
Chest 2004; 126:59-65
189
Phelan PD, Robertson CF, Olinsky A. The Melbourne Asthma Study: 1964-1999. J Allergy Clin
Immunol 2002; 109:189-194
190
James AL, Palmer LJ, Kicic E, Maxwell PS, et al. Decline in lung function in the Busselton Health
Study: the effects of asthma and cigarette smoking. Am J Respir Crit Care Med 2005; 171:109-114
191
Panizza JA, James AL, Ryan G, et al. Mortality and airflow obstruction in asthma: a 17-year follow-up
study. Intern Med J 2006; 36:773-780
192
Silva GE, Sherrill DL, Guerra S, Barbee RA. Asthma as a risk factor for COPD in a longitudinal study.
Chest 2004; 126:59-65
193
Xu X, Rijcken B, Schouten JP, et al. Airways responsiveness and development and remission of chronic
respiratory symptoms in adults. Lancet 1997; 350:1431-1434
194
McCloskey SC, Patel BP, Hinchcliff SJ, Reid ED, et al. Siblings of patients with severe chronic
obstructive pulmonary disease have a significant risk of airflow limitation. Am J Respir Crit Care Med
2001; 164:1419-1424
195
DeMeo DL, Carey VJ, Chapman HA, et al. Familial aggregation of FEF25-75 and FEF25-75/FVC in
families with severe, early onset COPD. Thorax 2004; 59:396-400
196
Tager IB, Segal MR, Speizer FE, Weiss ST. The natural history of forced expiratory volumes. Effect of
cigarette smoking and respiratory symptoms. Am Rev Respir Dis 1988; 138:837-849
197
Wong PM, Lees AN, Louw J, Lee FY, et al. Emphysema in young adult survivors of moderate to severe
bronchopulmonary dysplasia. Eur Respir J 2008. e-published April 2 2008, accessed 28 July 2008
41
TABLE 3.2. ENVIRONMENTAL RISK FACTORS FOR COPD198,199
Factor
Environmental
Factors
Cigarette smoking
Environmental tobacco smoke (incl parental
smoking)
Occupational dusts & fumes
Indoor/Outdoor air pollution (notably burning
of biomass fuels in poorly ventilated
buildings)
Dietary lack of anti-oxidants
Infections, and exacerbations
Socioeconomic status
Relationship & level of
evidence
Causal (II)200
Additive, or Causal if heavy
(III)201,202,203,204
Causal if heavy (IV)205
Additive, or Causal if heavy
(III)206,207
Additive (III)208
Additive (III)209
Additive (IV)210
Age
COPD is mainly a disease of the middle aged and the elderly. The peak prevalence of COPD has
been observed in the 45-64 and 65-74 age brackets211. Longitudinal data from the Tecumseh
study identified risk factors for developing COPD in a large population sample. Ages ranged
from 16-34 years at the start of the study to 30-80 years at follow up. The incidence of obstructive
airways disease (including asthma and chronic bronchitis) ranged from 4% in the 35-44 year age
group, to a peak of 16.3% in the 45-54 year age group in men. Men in the 55-64 year age group
198
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
199
Rabe KF, Hurd S, Anzueto A, et al. Global Strategy for the diagnosis, management, and prevention of
COPD: GOLD executive summary. Am J Respir Crit Care Med 2007; 176:532-555
200
US Surgeon General. The health consequences of smoking: chronic obstructive pulmonary disease. US
Department of Health and Human Services. Washington, DC: Publication No 84-50205, 1984
201
Leuenberger P, Schwartz J, Ackermann-Liebrich U, et al. Passive smoking exposure in adults and
chronic respiratory symptoms (SAPAL-DIA Study). Swiss Study on Air Pollution and Lung Diseases in
Adults, SAPALDIA Team. Am J Respir Crit Care Med 1994; 150:1222-1228
202
Eisner MD, Balmes J, Katz PP, Trupin L, et al. Lifetime environmental tobacco smoke exposure and the
risk of chronic obstructive pulmonary disease. Environ Health 2005; 4:7-10
203
Svanes C, Omenaas E, Jarvis D, et al. Parental smoking in childhood and adult obstructive lung disease:
results from the European Community Respiratory Health Survey. Thorax 2004; 59:295-302
204
De Marco R, Accordini S, Cerveri I, et al. An international survey of chronic obstructive pulmonary
disease in young adults according to GOLD Stages. Thorax 2004; 59:120-135
205
Kauffmann F, Drouet D, Lellouch J, Brille D. Twelve years spirometric changes among Paris area
workers. Int J Epidemiol 1979; 8:201-212
206
Samet JM, Marbury M, Spengler J. Health effects and sources of indoor pollution. Am Rev Respir Dis
1987; 136:1486-1508
207
Behera D, Jindal SK. Respiratory symptoms in Indian women using domestic cooking fuels. Chest
1991; 100:385-388
208
Guenegou A, Leynaert B, Pin I, et al. Serum carotenoids, vitamin A and E, and 8 year lung function
decline in a general population. Thorax 2006; 61:320-326
209
Miravitlles M, Ferrer M, Pont A, et al for the IMPAC Study Group. Effect of exacerbations on quality of
life in patients with chronic obstructive pulmonary disease: a 2 year follow up study. Thorax 2004; 59:387395
210
Prescott E, Lange P, Vestbo J. Socioeconomic status, lung function and admission to hospital for COPD:
results from the Copenhagen City Heart Study. Eur Respir J 1999; 13:1109-1114
211
Bakke PS, Baste V, Hanoa R, Gulsvik A. Prevalence of obstructive lung disease in a general population:
relation to title and exposure to some airborne agents. Thorax 1991;46:863-70
42
had an intermediate figure of 11.3%. In females there was less variation - 4.1% in the 35-44 year
age group, 5.0% in the 45-54 year age group, and 5.1% in the 55-64 year age group212. Data
from Europe show trends similar to the United States with highest prevalence rates of COPD
found in the older population. A study from the United Kingdom showed a prevalence of up to
16.4% in elderly populations213. In the United Kingdom, annual consultation rates for COPD per
10,000 population are highest for people aged 75 to 84214.
A review of the epidemiology of COPD (age- and gender-stratified prevalence rates in a
population that consisted of smokers as well as non-smokers) documented prevalence rates based
on physician confirmed diagnoses in males and females with FEV1/FVC < 75%. The prevalence
rates in men ranged from 2% in the 25-34 year age group to a peak of 24% in the 75+ age group.
In females, the prevalence rates were 2.5% in the 25-34 year age group and 4% in the 75+ age
group, with peak prevalence in females of 8.5% in the 55-65 year age group215.
Gender
Prevalence of COPD is generally found to be higher in men than in women. This may be due to
differences in smoking and occupational risks. With equivalent smoking, women may be at the
same or greater risk of developing COPD than men216. Data from the Beijing Respiratory Health
Study suggest that adverse effects of smoking on pulmonary function were greater in women than
in men, with similar rates of decline in lung function (and statistically different declines in FEV1
compared to non-smokers217. Data from two large population studies in Denmark also suggested
that smoking had a greater effect on lung function decline in females compared to males, and,
after adjusting for the level of smoking, females suffered a higher risk of hospital admission with
COPD than men218. In a Brazil 7-year prospective cohort study of people referred for long term
oxygen therapy, females had a statistically significantly higher risk of early death than men (after
accounting for age, nutrition and smoking)219.
Race/Ethnicity
In a study of Caucasian COPD patients in Canada, men of British origin were three times more
likely to have airflow obstruction than those of other North Eastern European ancestry, after
212
Higgins MW, Keller JB, Becker M, et al. An index of risk for obstructive airways disease. Am Rev.
Respir Dis. 1982; 125:144-151
213
Horsley JR, Sterling IJN, Waters WE, Howell JBL. Respiratory symptoms among elderly people in the
New Forest Area as assessed by postal questionnaire. Age and Aging, 1991; 20:325-31
214
Mak V. Chronic obstructive pulmonary disease (COPD). The UK perspective. Chest Medicine On-line.
1997; http://www.u-net.com/priory/cmol/copd.htm.
215
Sherrill DL, Lebowitz MD, Burrows B. Epidemiology of chronic obstructive pulmonary disease. Clin
Chest Med 1990;11:375-387
216
Chen Y, Horne SL, Dosman JA. Increased susceptibility to lung dysfunction in female smokers. Am Rev
Respir Dis 1991; 143:1224-1230
217
Xu X, Li B, Wang L. Gender difference in smoking effects on adult pulmonary function. Eur Respir J
1994;7:477-83
218
Prescott E, Bjerg AM, Andersen PK, et al. Gender difference in smoking effects on lung function and
risk of hospitalization for COPD: results from a Danish longitudinal population study. Eur Respir J
1997;10:822-7
219
Machado M-CL, Krishnan JA, Buist SA, et al. Sex differences in survival of oxygen-dependent patients
with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2006; 174:524-529
43
controlling for the effects of age and smoking220. The frequency of COPD in USA has been
unexpectedly low in African Americans, despite relatively high rates of smoking in this group,
though the reasons remain unexplained221; prevalence rates in this segment, though, are now
increasing222. Prevalence rates of COPD in Hispanic Americans living in New Mexico are
significantly lower than in Caucasians223, and after correcting for age and smoking exposure, the
prevalence of COPD is lower among Japanese American males than white males224. Asians have
generally been thought to have a lower susceptibility to COPD from smoking, though there may
be differences in type of tobacco used and the level of smoke inhaled, and allowing for these
factors decline in lung function fails to show consistent differences across races225.
Asthma and Airway Hyper-responsiveness
A Western Australian study was the first to present good data in 89 asthmatics, aged around 20,
to suggest asthma alone, independent of smoking, could result in fixed airflow limitation226. A
follow—up of this same population after 17 years showed better asthma control than previously,
with increased inhaled steroid use, but an even higher prevalence of chronic airflow limitation,
independent of smoking history227. There was a relatively high mortality rate (18 in 89 of these
now young-to-middle-aged adults). Other Australian studies have shown increased rate of decline
in FEV1228,229 and persistent airflow limitation post-bronchodilator230. Several other studies
support at least additive if not independently causative role for asthma in the development of
COPD231,232,233,234, and asthma and COPD may be comorbid or confounders of diagnosis235.
220
Horne SL, Cockcroft DW. Ethnicity as a possible factor contributing to the development of chronic
airflow limitation and asthma. Clin Invest Med 1990; 13:333-338
221
Coultas DB, Gong H, Grad R, et al. Respiratory Diseases in Minorities of the United States. Am J Respir
Crit Care Med 1993; 149:S93-S131
222
Bailey WC, Ferguson GT, Higgins M, et al for The National Lung Health Education Program Executive
Committee. Strategies in preserving lung health and preventing COPD and associated diseases. The
National Lung Health Education Program (NLHEP). Chest 1998; 113(Suppl):123S-163S
223
Samet JM, Coultas DB, Howard CA, Skipper BJ. Respiratory disease and cigarette smoking in a
Hispanic population in New Mexico. Am Rev Respir Dis 1988; 137:815-9
224
Beck GJ, Doyle CA, Schachter EN. Smoking and lung function. Am Rev Respir Dis 1981; 123:149-55
225
Oscherwitz M, Edlavitch SA, Baker TR, Jarboe T. Differences in pulmonary functions in various racial
groups. Am J Epidemiol 1972; 96:319-27
226
Brown PJ, Greville HW, Finucane KE. Asthma and irreversible airflow obstruction. Thorax 1984;
39:131-136
227
Panizza JA, James AL, Ryan G, et al. Mortality and airflow obstruction in asthma: a 17-year follow-up
study. Intern Med J 2006; 36:773-780
228
Peat JK, Woolcock AJ, Cullen K. Rate of decline of lung function in subjects with asthma. Eur J Respir
Dis 1987; 70:171-179
229
James AL, Palmer LJ, Kicic E, Maxwell PS, et al. Decline in lung function in the Busselton Health
Study: the effects of asthma and cigarette smoking. Am J Respir Crit Care Med 2005; 171:109-114
230
Phelan PD, Robertson CF, Olinsky A. The Melbourne Asthma Study: 1964-1999. J Allergy Clin
Immunol 2002; 109:189-194
231
Ulrik CS, Backer V, Dirksen A. A 10-year follow up of 180 adults with bronchial asthma: factors
important for the decline in lung function. Thorax 1992; 47:14-18
232
Lange P, Parner J, Vestbo J, et al. A 15-year follow-up study of ventilatory function in adults with
asthma. New Engl J Med 1998; 339:1194-1200
233
Hudson C, Turcotte H, Laviolette M, et al. Characteristics of bronchial asthma with incomplete
reversibility of airflow obstruction. Ann Allergy Asthma Immunol 1997; 78:195-202
234
Rasmussen F, Taylor DR, Flannery EM, Cowan JO, et al. Risk factors for airway remodelling in asthma
manifested by a low post-bronchodilator FEV1/vital capacity ratio: a longitudinal population study from
childhood to adulthood. Am J Respir Crit Care Med 2002; 165:1480-1488
44
Recent expert opinion from analysis of epidemiology and pathology suggests that a complex
genetic background to airways reactions to environmental perturbations may lead to either or both
asthma and COPD - altered innate immune responses cause progression of early airway damage
by tobacco smoke (and other noxious fumes and gases) to more obvious, symptomatic and severe
COPD through in turn inducing adaptive immune responses236. The hypothesis links bronchial
hyper-responsiveness with development of more severe stages of COPD.
Smoking
Most people with COPD have smoked over 20 pack-years (20 cigarettes per day or equivalent in
other forms of tobacco for 20 years), and smoking is said to contribute about 85% of the risk of
developing COPD237. However such data may be misleading, owing to the global misclassification problem with COPD, especially relating to death certification, where non-smoking
status contributes to under-attribution238. This is discussed in other Sections. The large
Copenhagen City Heart Study has indicated that after 25 years of smoking, at least 25% of
smokers without initial lung disease have clinically significant COPD, and 30-40% have all forms
of COPD; importantly early quitters did not develop COPD239. Incidence studies that examined
risk factors point to childhood smoking240,241,242, and also to bronchitic symptoms243,244. Parental
smoking has also been found as an independent risk factor for incidence of GOLD Stage II COPD
in some studies245,246, though not in others247. There is a clear demographic trend, with females as
they age showing more rapid decline in lung function than males248.
235
Bellia V, Battaglia S, Catalano F, et al. Aging and disability affect misdiagnosis of COPD in elderly
asthmatics. The SARA Study. Chest 2003; 123:1066-1072
236
Vestbo J, Hogg JC. Convergence of the epidemiology and pathology of COPD. Thorax 2006; 61:86-88
237
US Surgeon General. The Health Consequences of Smoking: Chronic Obstructive Lung Disease. US
Dept Health & Human Services. Washington, DC. DHHS Publication No 84-50205, 1984.
238
Meyer PA, Mannino DM, Redd SC, Olson DR. Characteristics of adults dying with COPD. Chest 2002;
122:2003-2008
239
Lokke A, Lange P, Scharling H, et al. Developing COPD: a 25 year follow up study of the general
population. Thorax 2006; 61:935-939
240
Gold DR, Wang X, Wypij D, et al. Effects of cigarette smoking on lung function in adolescent boys and
girls. N Engl J Med 1996; 223:931-937
241
Patel BD, Luben RN, Welch AA, et al. Childhood smoking is an independent risk factor for obstructive
airways disease in women. Thorax 2004; 59:682-686
242
Geijer RMM, Sachs APE, Verheij TJM, Salome PL, Lammers JWJ, Hoes AW. Incidence and
determinants of moderate COPD (GOLD II) in male smokers aged 40-65 years: 5-year follow up. Brit J
Gen Pract 2006; 56:656-661
243
Lingbergh A, Jonsson A-C, Ronmark E, et al. Ten-year cumulative incidence of COPD and risk factors
for incident disease in a symptomatic cohort. Chest 2005; 127:1544-1552
244
Geijer RMM, Sachs APE, Verheij TJM, Salome PL, Lammers J-WJ, Hoes AW. Incidence and
determinants of moderate COPD (GOLD II) in male smokers aged 40-65 years: 5-year follow up. Brit J
Gen Pract 2006; 56:656-661
245
Svanes C, Omenaas E, Jarvis D, et al. Parental smoking in childhood and adult obstructive lung disease:
results from the European Community Respiratory Health Survey. Thorax 2004; 59:295-302
246
De Marco R, Accordini S, Cerveri I, et al. An international survey of chronic obstructive pulmonary
disease in young adults according to GOLD Stages. Thorax 2004; 59:120-135
247
Geijer RMM, Sachs APE, Verheij TJM, Salome PL, Lammers J-WJ, Hoes AW. Incidence and
determinants of moderate COPD (GOLD II) in male smokers aged 40-65 years: 5-year follow up. Brit J
Gen Pract 2006; 56:656-661
248
Gan WQ, Man SFP, Postma DS, et al. Female smokers beyond the perimenopausal period are at
increased risk of chronic obstructive pulmonary disease: a systematic review and meta-analysis. Respir
Research 2006; 7:52-60
45
Biomass Smoke
The risk of developing chronic bronchitis is greater in populations exposed to indoor pollution
and smoke resulting from the use of stoves and heaters that utilize wood and coal as fuel. This
increase in risk is directly related to the length of the exposure to the smoke from the stoves.249 In
individuals who on average spend four or more hours daily in rooms with indoor pollution due to
heating or cooking with these stoves, the risk of developing chronic bronchitis is significantly
higher. In general, combustion of biomass fuel, including wood, charcoal, or dried dung
produces higher emission factors. This can lead to increased susceptibility to the development of
COPD, as compared to combustion of fossil fuels, including kerosene and gas.250 The prevalence
of indoor pollution from solid-fuel-fired cooking and heating stoves is widespread and this
exposure is said to be present in more than half the world’s households. A number of studies
from South Asia, including China, India, and Nepal, and a smaller number from Oceania, Latin
America, and Africa, have shown high indoor concentration of particulate matters, carbon
monoxide, and other pollutants which can cause decreased lung function.251 The prevalence of
COPD was higher by 30 to 60 percent in coal using homes as compared to homes that used gas
stoves. Women cooking more than three times per week, particularly if the frequency of heavy
cooking fumes is higher in the kitchen, have been reported to have decreased lung function.252
Occupational Exposure
Occupations involving a high exposure to airborne dusts during work have higher prevalence
rates of obstructive lung disease. Exposure to asbestos, quartz, wood dust, metal gases,
aluminium production and processing, and welding have been significantly associated with
obstructive lung disease, with greater risk observed after adjusting for the effects of age and
smoking253.
Workers in mining are exposed to dusts that may affect their lung function. Coal miners develop
bronchitis almost from the time of their entry into the mine, and the prevalence increases with
cumulative dust exposure254,255. Exposure to dust for workers in gold mining significantly
increases their risk of developing COPD and emphysema256. This has been observed in miners
who smoke, as well as in those who do not smoke cigarettes. Significant declines in lung function
have been observed in gold miners with exposure to smaller amounts of particulate matter in the
249
Perez-Padilla R, Regaldo J, Vedal S, et al. Exposure to bio-mass smoke and chronic airway disease in
Mexican women. A case controlled study. Am J Respir Crit Care Med 1996; 154(3 Pt 1):701-6
250
Zhang J, Smith KR. Hydrocarbon emissions and health risks from cookstoves in developing countries. J
Expo Anal Environ Epidemiol 1996;6(2):147-161
251
Chen BH, Hong CJ, Pandey MR, Smith KR. Indoor air pollution in developing countries. World Health
Stat Q 1990;43(3):127-138
252
Ng TP, Hui KP, Tan WC. Respiratory symptoms and lung function effects of domestic exposure to
tobacco smoke and cooking by gas in non-smoking women in Singapore. J Epidemiol Community Health,
1993;47(6):454-458
253
Korn RJ, Dockery DW, Speizer FE, et al. Occupational exposures and chronic respiratory symptoms. A
population-based study. Am Rev Respir Dis 1987; 136:298-304
254
Kibeltsis JA, Morgan EJ, Reger R, et al. Prevalence of bronchitis and airway obstruction in American
bituminous coal miners. Am Rev Respir Dis 1973; 108:886-893
255
Morgan WKC, Lapp NL. Respiratory disease in coal miners: State of the Art. Am Rev Respir Dis 1976;
113:531-559
256
Irwig L, Rocks P. Lung function and respiratory symptoms in silicotic and nonsilicotic gold miners. Am
Rev Respir Dis 1978; 117:429-435
46
dust, perhaps because of the increased silica content.257 Coke oven work in south-east China has
also been found to interact with smoking to increase risk of COPD258.
The prevalence of chronic bronchitis in workers exposed to dust from yarn and cement
manufacturing has been reported to be double that of individuals not exposed to these dusts259,260,
though this has been disputed261. A similar effect of more than doubled prevalence of chronic
bronchitis and decline in lung function has been reported in workers in the textile dyeing
industry.262 Workers in the Swedish paper manufacturing industry were found in a cross-sectional
study to have dose-dependent upper respiratory tract symptoms, but no increase in cough or
sputum production, but long-term heavy exposure did appear to be associated with lower lung
function263. Subsequent mortality study in this population confirmed higher prevalence rates of
death from asthma and COPD264.
In a study of over 10,000 farmers in Norway, it has been reported that full-time farming, livestock
production and exposure to associated dusts can increase the risk of chronic bronchitis and
significant decrease in lung function by 2 to 3 times. This risk can increase up to 6-fold if
combined with smoking.265 In a study of over 1,600 subjects in New Zealand, working with
vapours, gases, dust, or fumes was significantly associated with chronic bronchitis and airway
obstruction and could increase the risk of this outcome by 3 times.266 In Canada there are
powerful data supporting the risk of COPD from exposure to grain dust, especially among silo
workers, where epidemiological evidence is supported by experimental data267.
Environment (Air Pollution)
According to conservative estimates, moderate air pollution is expected to increase the prevalence
of chronic bronchitis by 25 percent.268 Moderate air pollution, defined in this Swiss study of
approximately 10,000 individuals from areas in Switzerland, is a 10 mcg/m3 increase in annual
mean particulate pollution (PM10). In a seminal Canadian series of studies where smoking rates
257
Oxman AD, Muir DC, Shannon HS, et al. Occupational dust exposure and chronic obstructive lung
disease. A systematic review of the evidence. Am Rev Respir Dis 1993; 148:38-48
258
Hu Y, Chen B, Yin Z, et al. Increased risk of chronic obstructive pulmonary disease in coke oven
workers: interaction between occupational exposure and smoking. Thorax 2006; 61:290-295
259
Arbons HL, Petersen MR, Sanderson WT, et al. Symptoms, ventilatory function, and environmental
exposures in Portland cement workers. Brit J Indust Med 1988; 45:368-375
260
Bergdahl IA, Toren K, Eriksson K, et al. Increased mortality in COPD among construction workers
exposed to inorganic dust. Eur Respir J 2004; 23:402-406
261
Bernstein DM. Increased mortality in COPD among construction workers exposed to inorganic dust.
Letter. Eur Respir J 2004; 23:512
262
Zuskin E, Mustajbegovic J, Schacter N, Doko-Jelinic D. Respiratory function of textile workers
employed in dyeing cotton and wool fibers. Am J Ind Med 1997; 31:344-352
263
Ericsson J, Järvholm B, Norin F. Respiratory symptoms and lung function following exposure in
workers exposed to soft paper tissue dust. Int Arch Environ Health 1988; 60:341-345
264
Thorén K, Järvholm B, Morgan U. Mortality from asthma and chronic obstructive pulmonary diseases
among workers in a soft paper mill: a case-referent study. Brit J Indust Med 1989; 46:192-195
265
Melbostad E, Eduard W, Magnus P. Chronic bronchitis in farmers. Scand J Work Environ Health
1997;23(4):271-80
266
Fishwick D, Bradshaw LM, D’Souza W, et al. Chronic bronchitis, shortness of breath, and airway
obstruction by occupation in New Zealand. Am J Respir Crit Care Med 1997;156(5):1440-1446
267
Zejda JE, McDuffie HH, Dosman JA. Respiratory effects of exposure to grain dust. Semin Respir Med
1993; 14:20-30
268
Kunzli N, Kaiser R, Rapp R, et al. Air pollution in Switzerland - quantification of health effects using
epidemiologic data. Schweiz Med Wochenschr 1997; 127(34):1361-1370
47
were standardised across the populations, a comparison of three cities found chronic bronchitis
was positively associated with air pollution269. In USA, a longitudinal study of never-smoking
Los Angeles residents revealed worse lung function in those exposed to higher levels of
photochemical oxidants, sulphates and particulates270. In a review of the health effects of outdoor
air pollution the American Thoracic Society attributed increased risk of development of COPD to
exposures to high levels of ambient pollution during adulthood, citing acid aerosols, total
suspended particulates and fine particulates (< 2.5 mcm)271. Health professionals in PR should
advocate for cleaner air to help their current clients and reduce the future impact of COPD272.
Socioeconomic Status
In the first US National Health and Nutrition Examination Survey report (NHANES I), low
income was a risk factor for COPD273. Patterns of environmental exposures affecting the lung
may differ depending on socioeconomic indicators such as housing characteristics, occupation
and lifestyle. In developed countries an inverse relationship between income/education and
prevalence of respiratory symptoms or disease can be shown274, although in 1,217 women in
Finland socioeconomic status was not related to the occurrence of respiratory disease275.
Nutrition
Oxidant injury appears to be a significant contributor to the damage resulting from inhalation of
toxic substances, and anti-oxidant intake might therefore modify initiation of COPD. Fresh fruit
intake has been positively associated with lack of respiratory (asthma) symptoms276, lung
function277, and lung function decline over time278. The 1995 Scottish Health Survey had reliable
results for all of: plasma levels of anti-oxidants, demographics, smoking history, dietary history,
respiratory symptoms and FEV1 in 1,146 randomly selected adults, and confirmed a doseresponse relationship between fresh fruit intake and pulmonary function, with vitamin E being
protective for symptoms of sputum production and vitamin C being protective for lung function
269
Bates DV. The fate of the chronic bronchitic: a report on the 10-year follow up in the Canadian
Department of Veterans Affairs coordinated study of chronic bronchitis: the J Burns Amberson Lecture of
the American Thoracic Society. Am Rev Respir Dis 1973; 108:1043-1065
270
Detels R, Tashkin DP, Sayre JW, Rokaw SN, et al. The UCLA population studies of chronic obstructive
respiratory disease. 9. Lung function changes associated with chronic exposure to photochemical oxidants;
a cohort study among never-smokers. Chest 1987; 92:594-603
271
A Committee of the Environmental and Occupational Health Assembly of the American Thoracic
Society. Health effects of outdoor pollution. Am J Respir Crit Care Med 1996; 153:3-50
272
Viegi G, Maio S, Pistelli F, et al. Epidemiology of chronic obstructive pulmonary disease: Health effects
of air pollution. Respirology 2006; 11:523-532
273
McWhorter WP, Polis MA, Kaslow RA. Occurrence, predictors, and consequences of adult asthma in
NHANESI and follow up survey. Am Rev Respir Dis 1989; 139:721-724
274
Lebowitz MD. The relationship of socio-environmental factors to the prevalence of obstructive lung
diseases and other chronic conditions. J Chronic Dis 1977; 30:599-611
275
Huhti E, Takala J, Nuutinen J, Poukkula A. Chronic respiratory disease in rural women. An
epidemiological survey at Hankasalmi, Finland. Ann Clin Res 1978; 10(2):95-101
276
Butland B, Strachan D, Anderson H. Fresh fruit intake and asthma symptoms in young British adults:
confounding or effect modification by smoking. Eur Respir J 1999; 13:744-750
277
Tabak C, Smit H, Rasanen L, etal. Dietary factors and pulmonary function: a cross sectional study in
middle aged men from three European countries. Thorax 1999;54:1021-1026
278
Carey I, Strachan D, Cook D. Effects of changes in fresh fruit consumption on ventilatory function in
healthy British adults. Am J Respir Crit Care Med 1998; 158:728-733
48
decline279. Smokers appear to have lower levels of serum anti-oxidants280, and low anti-oxidant
intake has been associated with lower FEV1 and more rapid decline of FEV1 with age281.
Conversely, French adults followed for 8 years had slower decline in FEV1 if they had higher Гџcarotene levels (and smoking plus low levels of Гџ-carotene or vitamin E imposed the greatest risk
of FEV1 decline)282. The Health Professionals Follow-up Study (HPFS) is a prospective cohort
dietary, lifestyle and health study of US health professionals aged 40-75 that began in 1986. Its
findings from 1986 to 1998 were recently published, and identified a diet rich in fruits, vegetables
and fish reduces the onset of COPD while a diet rich in refined carbohydrates, cured meats, red
meats, fried potatoes and desserts appeared to increase the risk of COPD283. Separating out the
influence of smoking and lifestyle from diet in developed populations may be difficult, but in
spite of increasingly consistent findings, it is surprising that guidelines for management of COPD
do not include discussion of dietary risk factors284.
Lung Growth
Bronchopulmonary dysplasia is the most significant long-term consequence of premature
parturition, with an increasing incidence of live births285. It affects up to 35% of very low birth
weight infants286. Lung growth is affected through childhood, and persistent lung function
abnormalities have been described287,288. Recent data have shown that as these individuals reach
adulthood they are at greater risk of abnormal computerised tomographic chest scan (CT)
characterised by airspace dilation and destruction (emphysema), and of abnormal gas transfer,
while over 68% of the cohort had features of airflow limitation – that is COPD appears to be
common in such individuals289,290, and further large-scale research of the incidence and
prevalence of this occurrence, and examination of methodsd to intervene, are needed.
279
Kelly Y, Sacker A, Marmot M. Nutrition and respiratory health in adults: findings from the Health
Survey for Scotland. Eur Respir J 2003: 21:664-471
280
Bolton-Smith C, Casey CE, Gey KF. Antioxidant vitamin intakes using a food frequency intakes
questionnaire: correlation with biochemical status in smokers and non-smokers. Br J Nutr 1991; 65:337346
281
Dow L, Tracey M, Villar A, et al. Does dietary intake of vitamin C and E influence lung function in
older people? Am J Respir Crit Care Med 1996; 154:1401-1404
282
Guenegou A, Leynaert B, Pin I, et al. Serum carotenoids, vitamin A and E, and 8 year lung function
decline in a general population. Thorax 2006; 61:320-326
283
Varraso R, Fung TT, Hu FB, Willett W, Camargo CA. Prospective study of dietary patterns and chronic
obstructive pulmonary disease among US men. Thorax 2007; 62:786-791
284
Celli BR, MacNee W, and committee members. Standards for the diagnosis and treatment of patients
with COPD: a summary of the ATS/ERS position paper. Eur Respir J 2004; 23:932-946
285
Tracy S, Tracy M, Dean J, et al. Spontaneous preterm birth of liveborn infants in women at low risk in
Australia over 10 years: a population based study. Brit J OG 2007; 114:731-735
286
Furman L, Baley J, Borawski-Clark E, et al. Hospitalization as a measure of morbidity among very low
birth weight infants with chronic lung disease. J Pediatr 1996; 128:447-452
287
Doyle LW, Cheung MM, Ford GW, et al. Birth weight <1501 g and respiratory health at age 14. Arch
Dis Child 2001; 84:40-44
288
Koumbourlis AC, Motoyama EK, Mutich RL, et al. Longitudinal follow-up of lung function from
childhood to adolescence in prematurely born patients with neonatal chronic lung disease. Pediatr
Pulmonol 1996; 21:28-34
289
Northway WH, Moss RB, Carlisle KB, Parker BR, et al. Late pulmonary sequelae of bronchopulmonary
dysplasia. N Engl J Med 1990; 323:1793-1799
290
Wong PM, Lees AN, Louw J, Lee FY, et al. Emphysema in young adult survivors of moderate to severe
bronchopulmonary dysplasia. Eur Respir J 2008. e-published April 2 2008, accessed 28 July 2008
49
COPD PREVENTION
KEY POINTS
The many environmental risk factors outlined indicate that COPD
is one of the most preventable diseases.
Primary prevention
smoking causes around 85% of the risk of COPD291
smoking is responsible for over 10% of global deaths (and is rising)292
preventing smoking initiation should be within the philosophical
framework of each health professional who deals with COPD
dietary anti-oxidants may be protective293
Western diet may increase risk of COPD
Secondary prevention
quitting smoking in the 25-44 year age-group eliminates risk of COPD
within the next 25 years294
smoking cessation is the only intervention shown to slow the natural
progression of the airflow limitation and its consequences295
3.3 Mortality
Population prevalence for COPD is less than for Asthma, but COPD causes more deaths. It is in
fact the fourth leading attributable cause of mortality in Australia, being registered as the primary
cause of death for 5,532 Australian in 1998296, and 4,886 in 2005297. COPD is the 4th most
291
US Surgeon General. The Health Consequences of Smoking: Chronic Obstructive Lung Disease. US
Dept Health & Human Services. Washington, DC. DHHS Publication No 84-50205, 1984
292
Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS
Med 2006; 3:2011-2030
293
Guenegou A, Leynaert B, Pin I, et al. Serum carotenoids, vitamin A and E, and 8 year lung function
decline in a general population. Thorax 2006; 61:320-326
294
Lokke A, Lange P, Scharling H, et al. Developing COPD: a 25 year follow up study of the general
population. Thorax 2006; 61:935-939
295
Fletcher C, Peto R. The natural history of chronic airflow obstruction. Brit Med J 1977; 1:1645-1648
296
Australian Institute of Health and Welfare. Australia’s Health 2000: the seventh biennial health report
of the Australian Institute of Health and Welfare. Canberra: AIHW; 2000
297
Australian Institute of Health and Welfare. Australia’s Health 2008; the eleventh biennial health report
of the Australian Institute of Health and Welfare. Ed P Magnus. AIHW cat. No AUS 99. Canberra: AIHW
2008
50
common cause of death in males and the 6th most common cause in females, with a steady or
declining death rate in males, but an increasing death rate in females298,299. In New Zealand
COPD is the 3rd most common cause of death in males and 4th most common in females. Death
rates in females were predicted to overtake those in men in around 2005300, and this is close to
being realized. A recent survey in the UK examined causes of death in patients with COPD from
1993 to 1999. COPD or asthma was listed in 312,664 death certificates (8.0% of total deaths), and
was the attributable cause of death in 59.8% of these. The main other causes of death in COPD
were acute myocardial infarction, non-infarct ischaemic heart disease and lung cancer, diseases
that share tobacco smoking as major risk factors301. It is likely that current population estimates
substantially understate the real mortality from COPD, as under-reporting on death certificates is
a major bias in such estimates302,303. Recent re-modelling from existing data has been applied by
the WHO Policy Cluster team, using three different sets of assumptions and “uncertainty
ranges”304. Total tobacco-attributable deaths are predicted to rise from 5.4 million in 2005 to 6.4
million in 2015 and 8.3 million in 2030, with COPD accounting for 27% of these. Respiratory
diseases is likely to undergo a 0.3% per annum average increase in age-standardised death rates
over that interval. Using these projections COPD will rise from 5th rank in causes of death
worldwide in 2002 to 4th rank in 2030. COPD will be responsible for 4.1% of deaths in high
income countries in 2030, 12.0% in middle income countries, and 5.5% in low income countries.
Risk Factors for and Predictors of Mortality
The progression of COPD is variable. Timed walking distance gradually deteriorated over three
years after PR, and the 3-year survival of patients with moderate and severe COPD was 80%305,
with a 6-years survival of 61%306. The risk factors for early mortality have been evaluated in a
number of longitudinal and retrospective studies. Severity of airflow limitation and pulmonary
hypertension307, severity of lung volume restriction created by dynamic hyperinflation308,309, rate
298
Australian Institute of Health and Welfare. Australia’s Health 2006; the tenth report of the Australian
Institute of Health and Welfare. Ed P Magnus. AIHW cat. No. AUS 73. Canberra: AIHW: pages 83-87
299
Wilson DH, Tucker G, Frith P, et al. Trends in hospital admissions and mortality from asthma and
chronic obstructive pulmonary disease in Australia, 1993-2003. Med J Aust 2007; 186:408-411
300
Crockett AJ, Cranston JM, Moss JR, Alpers JH. Trends in chronic obstructive pulmonary disease
mortality in Australia. Med J Aust 1994; 161:600-603
301
Hansell AJ, Walk JA, Soriano JB. What do chronic obstructive pulmonary disease patients die from? A
multiple cause coding analysis. Eur Respir J 2003; 22:809-814
302
Holguin F, Folch E, Redd SC, Mannino DM. Comorbidity and mortality in COPD-related
hospitalizations in the United States, 1979-2001. Chest 2005; 128:2005-2011
303
Jensen HH, Godtfredsen NS, Lange P, Vestbo J. Potential misclassification of causes of death from
COPD. Eur Respir J 2006; 28:781-785
304
Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS
Med 2006; 3:2011-2030
305
Gerardi DA, Lovett L, Benoit-Connors ML, Reardon JZ, ZuWallack RL. Variables related to increased
mortality following outpatient pulmonary rehabilitation. Eur Respir J 1996; 9:431-435
306
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995;
122:823-832
307
Traver GA, Cline MG, Burrows B. Predictors of mortality in chronic obstructive pulmonary disease. A
15-year follow-up study. Am Rev Respir Dis 1979; 119:895-902
308
Casanova C, Cote C, Torres JP, et al. Inspiratory-to-total lung capacity ratio predicts mortality in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2005; 171:591-597
309
Albuquerque ALP, Nery LE, Villaca DS, Machado TYS, et al. Inspiratory fraction and exercise
impairment in COPD patients GOLD stages II-III. Eur Respir J 2006; 28:939-944
51
of decline in spirometry310, level of hypoxaemia311, development of hypercapnic respiratory
failure312, severity of functional limitation313, continuing smoking314, nutritional status315, have all
been identified as risk factors. In five Nordic countries a prospective study of people admitted to
hospital for treatment of acute exacerbations of COPD identified 416 patients died in the 24
months of follow-up, with presence of diabetes being the risk factor with highest Hazard Risk
ratio (2.42; 95%CI=1.18-4.96) in addition to GOLD severity (HR 2.40), current smoking
(HR=1.73), comorbid cardiovascular disease (HR=1.52), age (HR=1.45) and previous
hospitalisations (HR=1.33)316.Depression, low quality of life, high levels of symptoms, functional
disability (low activity at home), and high exacerbation rates / hospitalization were good
predictors of one-year mortality in a British study of 100 consecutive patients admitted with
exacerbations317. Smoking is a risk factor both independently and through its effects on decline
rate of spirometry318,319 and on all-cause (especially cardiovascular) mortality. In-hospital
mortality for people admitted for acute exacerbations of COPD was linked to age, severity of
COPD, blood gas abnormalities, and complications arising during hospital stay320. Even the
presence of depression at admission for a hospitalisation for acute exacerbation of COPD has
been shown to be associated with worse survival321. Some of these factors have recently been
drawn together after multifactorial analysis and subsequent prospective validation into a BODE
Index, which emphasises body mass, spirometry, dyspnoea and exercise tolerance322.
3.4 Morbidity and Burden of Illness
Burden of illness refers to the combined effects of mortality and morbidity from chronic health
conditions. The WHO and World Bank have developed a summary measure of burden of illness
310
Postma DS, Sluiter HJ. Prognosis of chronic obstructive pulmonary disease: The Dutch experience. Am
Rev Respir Dis 1989; 140 (Suppl):S100-S105
311
The Medical Research Council Working Party. Long term domiciliary oxygen therapy in chronic
hypoxaemic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981; 1:681-686
312
Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic
obstructive pulmonary disease: A clinical trial. Ann Intern Med 1980; 93:391-398
313
Bowen JB, Votto JJ, Thrall RS, Haggerty MC, et al. Functional status and survival following pulmonary
rehabilitation. Chest 2000; 118:697-703
314
Hersh CP, DeMeo DL, Al-Ansari E, Carey VJ, et al. Predictors of survival in severe, early onset COPD.
Chest 2004; 126:1443-1451
315
Landbo C, Prescott E, Lange P, Vestbo J, Almdal TP. Prognostic value of nutritional status in chronic
obstructive pulmonary disease. Am J Respir Crit Care Med 1999; 160:1856-1861
316
Gudmunsson G, Gislason T, Lindberg E, Hallin R, et al. Mortality in COPD patients discharged from
hospital: the role of treatment and co-morbidity. Respir Research 2006; 7:109-116
317
Yohannes AM, Baldwin RC, Connolly MJ. Predictors of 1-year mortality in patients discharged from
hospital following acute exacerbation of chronic obstructive pulmonary disease. Age Ageing 2005; 34:491496
318
Fletcher C, Peto R. The natural history of chronic airflow obstruction. Brit Med J 1977; 1:1645-1648
319
Anthonisen NR, Skeans MA, Wise RA, Manfred J, et al. The effects of a smoking cessation intervention
on 14.5-year mortality. A randomized clinical trial. Ann Intern Med 2005; 142:233-239
320
Bustamante-Fermosel A, De Miguel-Yanes JM, Duffort-Falco M, Munoz J. Mortality-related factors
after hospitalization for acute exacerbations of chronic obstructive pulmonary disease: the burden of
clinical features. Am J Emerg Med 2007; 25:515-522
321
Ng T-P, Niti M, Tan W-C, Cao Z, et al. Depressive symptoms and chronic obstructive pulmonary
disease. Effect on mortality, hospital readmission, symptom burden, functional status, and quality of life.
Arch Intern Med 2007; 167:60-67
322
Celli BR, Cote CG, Martin JM, et al. The BMI, airflow obstruction, dyspnoea and exercise capacity
index in COPD. New Engl Med J 2004; 350:1005-1012
52
due to premature death (years of life lost due to premature mortality – YLL) and disability (years
of healthy life lost due to poor health or disability – YLD). Adding these, weighting for societal
preferences for different health states, and applying an annual discount to account for the natural
decline in activity, productivity and perceived health with age provides Disability Adjusted Life
Years – DALYs323. International and Australian data show that COPD ranks fourth in males for
DALYs and sixth in females in most developed nations. Worldwide, COPD currently ranks
twelfth for DALYs, though WHO projects that it will rank fifth in 2020, due largely to dramatic
increases in use of tobacco in developing nations and improving life expectancy324.
WHO has recently re-assessed the projections in mortality and morbidity through to 2030325.
DALY rankings predict COPD will rise from 11th in 2002 to 7th in 2030, and indicate it will be
responsible for 2.5% of DALYs in high income countries at that time, 4.7% in middle income
countries, and fewer than 2.5% in low income countries.
Other terms developed or suggested to account for inadequacies in QALYs and DALYs have not
been well validated. One index specific to Australia is the Body Burden of Disease (BBD)326,
which refers to the number of body systems affected by the disease. The International
Classification of Disease (ICD-9-CM) defines 23 body system (but not necessarily organ system)
categories, and BBD can therefore range from 1 to 23 in any individual. Its utility was evaluated
in a hospital population of 21,877 patients327. BBD is one factor predicting hospital length of stay
and death, though its contribution varied across major diagnostic categories. The usefulness of
BBD based on the more recent ICD-10-AM, and in a broader context, needs further examination.
3.5 Costs
American Medicare beneficiaries with COPD have 2.5 times the expenditure of beneficiaries
without COPD, with total costs for COPD care in 1993 for US being $US23.9 billion (61.5%
direct costs, 18.8% due to mortality, and 19.7% due to morbidity328). Studies in the UK using a
,
“top-down” analysis of administrative costs329 330, or “bottom-up” microcosting suggest total
annual costs of ₤781-1,154 per patient (AUD 1,950-2,900)331. The annual costs (direct + indirect)
were ₤800-1,500 million, most attributed to care of patients with severe COPD.
There are other important though unquantified cost impacts that should not be overlooked. One is
depression (between 30 and 96% of patients with COPD display anxiety, depression, panic,
323
Murray CJL, Lopez AD, Eds. The global burden of disease: a comprehensive assessment of mortality
and disability from diseases, injuries and risk factors in 1990 and projected to 2020. Cambridge, MA:
Harvard University Press; 1996
324
Murray CJL, Lopez AD. Evidence-based health policy - lessons from the Global Burden of Disease
Study. Science 1996; 274:740-743
325
Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS
Med 2006; 3:2011-2030
326
Roe CJ, Kulinskaya E, Dodich N, Adam WR. Comorbidities and prediction of length of hospital stay.
Aust NZ J Med 1998; 28:811-815
327
Roe CJ, Kulinskaya E, Dodich N, Adam WR. ibid
328
Grasso ME, Weller WE, Shaffer TJ, Diette GB, Anderson GF. Capitation, managed care, and chronic
obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 158:133-138
329
Guest JF. The annual cost of chronic obstructive pulmonary disease to the UK’s National Health
Service. Dis Manage Health Outcomes 1999; 5:93-100
330
Sullivan SD, Ramsey SD, Lee TA. The economic burden of COPD. Chest 2000; 117:5S-9S
331
Britton M. The burden of COPD from the confronting COPD survey. Respir Med 2003; 97:S71-S79
53
confusion or neurosis). Another is the economic and emotional burden on carers. Third, as the
disease progresses and impairments advance, other organ systems are threatened by
complications and concurrent morbidities related to smoking and older age. None of these costs is
accounted in costs of COPD. The ALF extrapolated from US statistics that the annual direct and
indirect costs of COPD to the Australian community were almost AUD800 million332.
Direct Costs
These are the financial costs of health care resources for diagnosing and treating the condition. As
detailed by the AIHW333, Respiratory Diseases are the sixth most costly disease group in
Australia, accounting for $2.5 billion, or 8.0% of total health system costs. Each year in Australia,
over 40,000 hospital separations have the principal diagnosis of COPD, with an average length of
stay of 5.3 days. In 1993-1994 the direct health system costs in Australia for COPD were $300
million.
According to the US National Medical Expenditure Survey (1993) around 73% of direct
expenditure in USA for COPD patient care was for 10% of the patients, and 72.8% of the costs of
overall illness burden were for hospital admissions and emergency department presentations.
Outpatient or clinic/office visits represented 15% and prescription drugs around 12%334. The
health system in Australia places emphasis on a robust primary care sector, and the breakdowns
may be different. Unlike asthma, where most of the costs are associated with pharmaceuticals to
control the disease, in COPD over 35% of the direct costs are associated with hospitalisation
(Table 3.3).
TABLE 3.3.
DIRECT COSTS OF COPD IN AUSTRALIA, 1993-1994 AND 2000-2001335
Cost segment
Hospital
Medical
Pharmaceuticals (prescribed & OTC)
Other
TOTAL
1993-1994
$112 million
$ 61 million
$ 66 million
$ 61 million
$300 million
2000-2001
$188 million
$102 million
$111 million
$102 million
$503 million
Indirect Costs
These costs derive from missed schooling or employment by the patient or carer, premature
death, and other costs related to disablement; social security payments are not usually included
because these are intra-population transfers (from tax-payers to recipients of benefits)336. Costs to
the healthcare system therefore do not reflect the total cost of COPD to the community. COPD
has other significant economic impacts, such as absenteeism, productivity losses and change of
duties leading to early retirement. Within 7 to 8 years of initial diagnosis, most people with
332
Crockett AJ, Cranston JM, Moss JR. Economic Case Statement. Chronic obstructive pulmonary disease
(COPD). The Australian Lung Foundation; 2002
333
Australian Institute of Health and Welfare. Australia’s Health 2000: the seventh biennial health report
of the Australian Institute of Health and Welfare. Canberra: AIHW; 2000
334
Sullivan SD, Strassels SA, Smith DH. Characterization of the costs of chronic obstructive pulmonary
disease (COPD) in the US. Eur Respir J 1996; 9 (Supp 23):421S
335
Crockett AJ, Cranston JM, Moss JR. Economic Case Statement. Chronic obstructive pulmonary disease
(COPD). The Australian Lung Foundation; 2002
336
Robinson R. Economic evaluation and health care: what does it mean? Br Med J 1993; 307:670-673
54
COPD are no longer capable of productive work337. In the UK it has been estimated that 44% of
people with COPD are within their working years, and these working patients lost on average
almost two weeks’ work each year338. AIHW figures do not reflect these indirect costs.
COPD EPIDEMIOLOGY - KEY POINTS
1)
The major risk factor for COPD is tobacco smoking
2)
A quarter of all smokers have significant respiratory symptoms
3)
COPD occurs in at least 12% of adults over 45
4)
COPD ranks 4th as a leading cause of mortality in Australia
5)
COPD ranks 3rd or 4th for burden of illness in developed nations
6)
COPD will rank 5th globally for burden of illness by 2020
7)
COPD increases in prevalence with age
8)
COPD is increasing in women
9)
Respiratory diseases account for 8% of Australia's health costs
10)
COPD admissions in Australia cost over $AU300 million pa
11)
Indirect costs for COPD are $AU500 million pa
3.6 Carer Burden
The bulk of long term care of people with many chronic conditions is undertaken by informal
carers, who are usually family members. Recognition of this role has been made in conditions
such as dementia and Alzheimer’s disease, depression, neurological disease including strokes,
and in cancer. The psychosocial health of carers of people with dementia has been compared with
that of older persons attending their general practitioners and of people with disabling arthritis
and other conditions339. The carers were as restricted in social and recreational activities as the
arthritis sufferers, though not as much as dialysis patients. In an Australian study, full-time carers
337
Goldring JM, James DS, Anderson HA. Chronic lung diseases. In: Brownson R, Remington PL, David
JR, Eds. Chronic Disease Epidemiology and Control. Washington DC: American Public Health
Association; 1993.
338
Britton M. The burden of COPD from the confronting COPD survey. Respir Med 2003; 97:S71-S79
339
LoGiudice D, Kerse N, Brown K, Gibson SJ, et al. The psychosocial health status of carers of persons
with dementia: a comparison with the chronically ill. Qual Life Res 1998; 7:345-351
55
of elderly people had more mental symptoms and worse life satisfaction than part-time carers. In
particular, if the full-time carer felt controlled by the elderly person, carer distress was worse340.
While the burden of caring for people with chronic diseases has been acknowledged, and both
physical and mental health problems have been ascribed to this role, measures of burden of
disease, such as DALYs, do not include health and well-being of carers.
In non-respiratory populations, the psychological health of carers and patients are linked341. No
matter how intensive the caring role may be, carers suffer significant emotional distress in part
due to the health of their patient and in part due to their inability to participate in their own
activities and past-times342. Levels of loneliness, social isolation and depression were similar
among carers and their patients343. The quality of care received by the patient from family carers
is linked with health of the carer, and carer health status has been found to be associated with
rates of health care utilisation by their patients344. Caregivers and patients are often found to
communicate their fears and anxieties ineffectively345, and actually avoid conversations around
their concerns about the rate of decline of their patient346, often specifically to avoid
psychological distress for them and their patient. Caregivers, though, actually prefer to have more
communication about their patient’s illness, both with the physician and the patient347,348.
Education interventions and other supports may be useful in alleviating carer burden and
improving the quality of patient care. Provision of guidelines to carers, formal teaching and
specific family intervention have improved patient care, delayed nursing home placement, or
reduced health care usage349,350,351. Based on such observations, it has been suggested that a
preventive approach with development of formal and informal supports for carers should be
adopted, with training and education aimed at improving patient care and reducing carer
burden352.
340
Broe GA, Jorm AF, Creasey H, Casey B, et al. Carer distress in the general population: results from the
Sydney Older Persons Study. Age Ageing 1999; 28:307-311
341
Jones DA, Peters TJ. Caring for elderly dependents: effects on the carers' quality of life. Age & Ageing
1992; 21:421-428
342
Cameron JI, Franche RL, Cheung AM, et al. Lifestyle interference and emotional distress in family
caregivers of advanced cancer patients. Cancer 2002; 94:521-527
343
Keele-Card G, Foxall MJ, Barron CR. Caring for elderly dependents: effects on the carers’ quality of
life. Publ Health Nurs 1993; 10:245-251
344
Draper B, Luscombe G. Quantification of factors contributing to length of stay in an acute
psychogeriatric ward. Internat J Geriatric Psychiatry 1998; 13:1-7
345
Zhang AY, Siminoff LA. Silence and cancer: Why do families and patients fail to communicate? Health
Commun 2003; 15:415-429
346
Pecchioni LL. Implicit decision-making in family caregiving. J Soc Personal Relationships 2001:
18:219-237
347
Hanson LC, Danis M, Garrett J. What is wrong with end-of-life care ? Opinions of bereaved family
members. J Am Geriatr Soc 1997; 45:1339-1344
348
Fried TR, Bradley EH, O’Leary JR, Byers AL. Unmet need for caregiver-patient communication and
increased caregiver burden. J Am Geriatr Soc 2005; 53:59-65
349
Evans RL, Matlock AL, Biship DS, Stranahan S, Pedersen C. Family intervention after stroke: does
counselling or education help? Stroke 1998; 19:1234-1239
350
Roy R, Thomas M, Cook A. Social context of elderly chronic pain patients. In: Ferrell BR, Ed. Pain in
the Elderly. Seattle: IASP Press; 1996: pp111-117S
351
Mittleman MS, Ferris SH, Shulman E, Steinberg G, Levin B. A family intervention to delay nursing
home placement of patients with Alzheimer’s disease. JAMA 1996; 276:1725-1731
352
Schofield H, Bloch S. Disability and chronic illness: the role of the family carer. Med J Aust 1998;
169:405-406
56
Carers are critical to and are often bound up in care of respiratory patients, and this results in
physical and emotional health problems353. Parents of children with asthma, for example, are
central carers for their child, yet in a prospective randomised partially blinded controlled trial
provision of guided self-management principles to the parents yielded no significant benefits in
health care utilisation, disability score of the children, or carers' quality of life354. The carer
burden for parents of children with severe asthma is likely to differ from that for spouses of
patients with severe COPD. The former condition is usually more intermittent and attacks can be
severe and highly emotionally charged. Carers of people with more chronic symptoms of
schizophrenia, for example, use different coping styles, especially passivity, than carers of people
with more episodic schizophrenia355. Carers of children with asthma are younger than carers of
people with COPD, and carer age, gender, health and cognitive function are significant predictors
of carer stress356,357,358.
Few formal studies about carers of COPD patients have been published, though Australian data
from controlled studies suggested significant relationships in the psychological health status
between patients with COPD and their carers, supporting the involvement of the care dyad in
respiratory management planning359. They also indicated that the handicap experienced by carers
of patients with other chronic illnesses occurs in carers of patients with COPD, and that an
improvement in patients’ self-management through completion of PR may reduce the handicap
associated with the carer’s role and may also benefit the mental health of the carer360. Carers
themselves reported improved psychological health and social adjustment for their patients
following PR, in line with what patients themselves report361. In a recent US study, patients with
COPD and their life partners had high levels of marital adjustment, associated with better quality
of life for the patient and better physical functioning for the spouse. Those with poor marital
adjustment responded more favourably to PR than did well-adjusted patients362
If education can help carers provide better care with reduced stress, it appears logical for sessions
for carers to be included in PR programs. Carers should at least be encouraged to attend PR
programs with their patient, and to become members of Support Groups (SG). However, there is
no objective evidence to support (or refute) such recommendations.
353
Clark GS, Siebens HC. Geriatric rehabilitation. In: DeLisa JA, Gans BM, Eds. Rehabilitation Medicine,
3rd edition. Philadelphia PA: Lippincott-Raven; 1998
354
Stevens CA, Wesseldine LJ, Couriel JM, Dyer AJ, et al. Parental education and guided self-management
of asthma and wheezing in the pre-school child: a randomised controlled trial. Thorax 2002; 57:39-44
355
Bibou-Nakou I, Dikiaou M, Bairactaris C. Psychosocial dimensions of family burden among two groups
of carers looking after psychiatric patients. Soc Psychiatry Psychiatric Epidemiol 1997; 32:104-108
356
Hodgson SP, Wood VA, Langton-Hewer R. Identification of stroke carers "at risk": a preliminary study
of carers' psychological well-being at one year post stroke. Clin Rehabil 1996; 10:337-346
357
Knight RG, Devereux RC, Godfrey HPD. Psychosocial consequences of caring for a spouse with
multiple sclerosis. J Clin Exper Neuropsychol 1997; 19:7-19
358
Cullen JS, Grayson DA, Jorm AF. Clinical diagnoses and disability of cognitively impaired older
persons as predictors of stress in their carers. Internat J Geriatric Psychiatry 1997; 12:1019-1028
359
Cafarella P, Frith P. Psychological status of COPD patients and their carers are linked. Respirology
2001; 6(Suppl):A36
360
Cafarella P, Frith P. Patient completion of pulmonary rehabilitation reduces carer handicap. Respirology
2001; 6(Suppl):A35
361
Cafarella P, Frith P. Pulmonary rehabilitation reduces carer strain and psychological morbidity.
Respirology 2000; 5(Suppl):A43
362
Ashmore JA, Emery CF, Hauck ER, MacIntyre NR. Marital adjustment among patients with chronic
obstructive pulmonary disease who are participating in pulmonary rehabilitation. Heart Lung 2005;
34:270-278
57
3.7 Assessing COPD Severity
Guidelines of management of COPD have varying definitions of COPD severity, but by
international agreement the GOLD Strategy363 developed a classification of stages of disease
based originally on FEV1 alone. Recent modifications have included symptom severity and
presence of complications or systemic consequences364. Evidence supporting one or other
classification of severity is at present lacking. The TSANZ guidelines (known as �COPD-X’)365
utilise several indexes relating to severity, from FEV1 levels to HRQoL impairment and severity
of dyspnoea366, because the degree of dyspnoea rating predicts exercise impairment, mood
disturbance and health status367 (Table 3.4). The relevance of the COPD-X severity gradings to
patient functionality has been challenged, however368.
363
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
364
Rabe KF, Hurd S, Anzueto A, et al. Global Strategy for the diagnosis, management, and prevention of
COPD: GOLD executive summary. Am J Respir Crit Care Med 2007; 176:532-555
365
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
366
Hajiro T, Nishimura K, Tsukino M, et al. Stages of disease severity and factors that affect the health
status of patients with chronic obstructive pulmonary disease. Respir Med 2000; 94:841-846
367
Bestall JC, Paul EA, Garrod R, et al. Usefulness of the Medical Research Council (MRC) dyspnoea
scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 1999;
54:581-586
368
Kyoong, Mol S, Guy P, Finlay P, et al. Comparison of Australian and international guidelines for
grading severity of chronic obstructive pulmonary disease. Intern Med J 2006; 36:506-512
58
TABLE 3.4.
COPD-X CLASSIFICATION OF SEVERITY STAGES IN COPD369
Stage
0:
At Risk
I:
Mild COPD
II:
Moderate COPD
III:
Severe COPD
IV:
Very severe
COPD
Spirometry
Criteria
Normal
(FEV1/FVC>0.7
and FEV1>80%
predicted
FEV1/FVC<0.7
but FEV1>80%
predicted
FEV1/FVC<0.7
and FEV1 60% to
80% predicted
Clinical Criteria
Other features
Chronic symptoms of cough
or sputum production
Presence of risk factors
Usually but not always
chronic cough or sputum
production
Chronic symptoms of cough,
sputum production and
shortness of breath on
exertion
Chest Xray and complex lung function
tests often normal
FEV1/FVC<0.7
and FEV1 40% to
60% predicted
FEV1/FVC<0.7
and FEV1 below
40% predicted
Deteriorating quality of life
with limitation of normal
activities
Quality of life severely
impaired with severe
breathlessness, intractable
coughing, and/or lifethreatening exacerbations
Patients start to seek medical attention
with shortness of breath or
exacerbations of disease. Chest Xray
often shows hyperinflation, and
DCO<70% predicted
As above
Respiratory Failure (pO2<60 mmHg
and/or pCO2>50 mmHg).
Signs of right heart failure (raised JVP,
ankle oedema).
3.8 Exacerbations of COPD
The term exacerbation has been difficult to define and to quantitate, but it is especially important
to have an operational definition when research questions that relate to reducing exacerbations are
being considered. Characteristics of exacerbations include a change in symptoms of cough,
sputum or dyspnoea, change in overall health status, and a need for change in treatment. Variable
elements of airway inflammation are usually (but not universally) evident.
Given the importance of exacerbations in the lives of people with COPD (and their carers) it has
been useful to develop a standardised working definition of acute exacerbation of COPD: “an
event in the natural course of COPD that is characterised by a sustained worsening in the patient’s
condition of the stable state beyond normal day-to-day variations, such as dyspnoea, cough, or
sputum, and necessitates a change in regular management.”370,371
Exacerbations are more common in moderate and severe COPD372,373. They are one of the most
important contributors to worsening quality of life374,375,376. In turn, worse quality of life was a
369
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
370
Rodriguez-Roisin R. Towards a consensus definition for COPD exacerbations. Chest 2000; 117:398S401S
371
Celli BR, MacNee W. Standards for the diagnosis and treatment of patients with COPD: a summary of
the ATS/ERS position paper. Eur Respir J 2004; 23:932-946
372
Seemungal TA, Donaldson GC, Bhowmik A, et al. Time course and recovery of exacerbations in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000; 161:1608-1613
373
Connors AF, Dawson NV, Thomas C, et al. Outcomes following acute exacerbation of severe chronic
obstructive lung disease. The SUPPORT investigators (Study to Understand Prognoses and Preferences for
Outcomes and Risks of Treatment). Am J Respir Crit Care Med 1996; 154:959-967
59
more important predictor of hospital readmission for COPD than airway physiology377.
Exacerbations frequently result in critically altered ventilatory mechanics as a result of dynamic
hyperinflation leading to the dyspnoea that triggers presentation to hospital, and onset of
respiratory failure378.
The airways of people with moderate and severe COPD are often colonised by Haemophilus
influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and other bacteria379,380,381.
Colonisation increases the rate of exacerbations382 but bacterial counts, changes in bacterial
strains383 and greater airway inflammation384 correlate with each other during exacerbations. The
other major triggers are viral385,386,387 (especially rhinovirus) with increased airway
inflammation388, and are associated with increased respiratory and all-cause mortality389.
Increased rates of exacerbations are usually more common in winter months, though even in very
cold regions, as long as adequate indoor heating and wearing of appropriate clothes are provided,
this seasonal variation is surprisingly less evident390,391. Indeed, in countries with warmer average
374
Seemungal TA, Donaldson GC, Paul EA, et al. Effect of exacerbation on quality of life in patients with
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157:1418-1422
375
Wang Q, Bourbeau J. Outcomes and health-related quality of life following hospitalisation for and acute
exacerbation of COPD. Respirology 2005; 10:334-340
376
Miravitlles M, Ferrer M, Pont A, Zalacain R, et al, for the IMPAC Study Group. Effect of exacerbations
on quality of life in patients with chronic obstructive pulmonary disease: a 2 year follow up study. Thorax
2004; 59:387-395
377
Osman IM, Godden DJ, Friend JA, et al. Quality of life and hospital re-admission in patients with
chronic obstructive pulmonary disease. Thorax 1997; 52:67-71
378
O’Donnell DE, Parker CM. COPD exacerbations. 3: Pathophysiology. Thorax 2006; 61:354-361
379
Monso E, Rosell A, Bonet G, Manterola J, et al. Risk factors for lower airway bacterial colonization in
chronic bronchitis. Eur Respir J 1999; 13:338-342
380
Zalacain R, Sobradill V, Amilibia J, Barron J, et al. Predisposing factors to bacterial colonization in
chronic obstructive pulmonary disease. Eur Respir J 1999; 13:343-348
381
Stockley RA, O’Brien C, Pye A, Hill SL. Relationship of sputum color to nature and outpatient
management of acute exacerbations of COPD. Chest 2000; 117:1638-1645
382
Sethi S, Maloney J, Grove L, et al. Airway inflammation and bronchial bacterial colonization in chronic
obstructive pulmonary disease. Am J Respir Crit Care Med 2006; 173:991-998
383
Chin CL, Manzel IJ, Lehman EE, Humlicek AL, et al. Haemophilus influenzae from COPD patients
with exacerbation induce more inflammation than colonizers. Am J Respir Crit Care Med 2005; 172:85-91
384
Wilkinson TM, Patel IS, Wilks M, et al. Airway bacterial load and FEV1 decline in patients with
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2003; 167:1090-1095
385
Seemungal TA, Harper-Owen R, Bhowmik A, et al. Detection of rhinovirus in induced sputum at
exacerbation of chronic obstructive pulmonary disease. Eur Respir J 2000; 16:677-683
386
Seemungal TA, Harper-Owen R, Bhowmik A, Moric I, et al. Respiratory viruses, symptoms, and
inflammatory markers in acute exacerbations and stable chronic obstructive pulmonary disease. Am J
Respir Crit Care Med 2001; 164:1618-1623
387
Rohde H, Wiethege A, Borg I, Kauth M, et al. Respiratory viruses in exacerbations of chronic
obstructive pulmonary disease requiring hospitalisation: a case-control study. Thorax 2003; 58:37-42
388
Bhowmik A, Seemungal TA, Sapsford RJ, Wedzicha JA. Relation of sputum inflammatory markers to
symptoms and lung function changes in COPD exacerbations. Thorax 2000; 55:114-120
389
Wilkinson TM, Pattenden S, Armstrong B, et al. Vulnerability to winter mortality in elderly people in
Britain: population based study. Brit Med J 2004; 329:647-653
390
Donaldson GC, Tchernjavskii VE, Ermakov SP, et al. Winter mortality and cold stress in Yekaterinburg,
Russia: interview study. Brit Med J 1998; 316:514-518
391
Donaldson GC, Ermakov SP, Komarov YM, et al. Cold related mortalities and protection against cold in
Yakutsk, eastern Siberia: observation and interview study. Brit Med J 1998; 317:978-982
60
temperatures, the mortality from winter cold-related exacerbations is greatest392. It is logical to
suggest that reduced exacerbations might be achievable through better heating for the aged and
infirm during winter months, especially in more temperate climates.
Air pollution is a significant risk factor for exacerbations of COPD. Higher rates of mortality
and/or hospitalisation (all-cause, cardiac and respiratory) are associated with higher levels of
small particle, sulphur dioxide or nitrogen dioxide pollution393,394,395,396, and pollution increases
markers of airways inflammation. Diesel exhaust, for example, increases airway inflammatory
markers397,398,399.
Although there is increasing consensus on the definition of exacerbations of COPD (see above),
the aetiologies, symptoms and treatments are heterogeneous. Additionally, the severity of an
exacerbation may be hard to classify. Classifications and definitions that rely on symptoms may
be unreliable, and this may impact on evaluation of treatments for exacerbations. Since
inflammation is considered to be the root cause of exacerbated symptoms, there is logic in finding
reliable markers of inflammation that might be used to detect and monitor exacerbations. To that
end, a systematic research review was recently undertaken with meta-analysis400. Among the 268
research reports (investigating 142,407 patients with COPD) the authors based their severity
classification on simple ATS/ERS criteria (Level I – suitable for home management – Level II –
requires hospitalisation – Level III – requires specialised care). Of the hundreds of measures
examined in these studies, the most consistent markers correlating with severity rating were
arterial pCO2 and respiration rate. If exacerbations can be prevented with appropriate therapies
(see below) overall health status can be improved401, and self-management of exacerbations
should be part of patient education.
392
Eurowinter Group. Cold exposure and winter mortality from ischaemic heart disease, respiratory
disease, and all causes in warm and cold regions of Europe. Lancet 1997; 349:1341-1346
393
Sunyer J, Saez M, Murillo C, Castellsague J, et al. Air pollution and emergency room admissions for
chronic obstructive pulmonary disease: a 5-year study. Am J Epidemiol 1993; 137:701-705
394
Anderson HR, Spix C, Medina S, Schouten JP, et al. Air pollution and daily admissions for chronic
obstructive pulmonary disease in 6 European cities: results from the APHEA project. Eur Respir J 1997;
10:1064-1071
395
Garcia-Aymerich J, Tobias A, Anto JM, Sunyer J. Air pollution and mortality in a cohort of patients
with chronic obstructive pulmonary disease: a time series analysis. J Epidemiol Community Health 2000;
54:73-74
396
Sunyer J, Schwartz J, Tobias A, Macfarlane D, et al. Patients with chronic obstructive pulmonary
disease are at increased risk of death associated with urban particle air pollution: a case-crossover analysis.
Am J Epidemiol 2000; 151:50-56
397
Ohtoshi T, Takizawa H, Okazaki H, Kawasaki S, et al. Diesel exhaust particles stimulate human airway
epithelial cells to produce cytokines relevant to airway inflammation in vitro. J Allergy Clin Immunol 1998;
101:778-785
398
Rudell B, Blomberg A, Helleday R, Ledin MC, et al. Bronchoalveolar inflammation after exposure to
diesel exhaust: comparison between unfiltered and particle trap filtered exhaust. Occup Environ Med 1999;
56:527-534
399
Nordenhall C, Pourazar J, Blomberg A, Levin JO, et al. Airway inflammation following exposure to
diesel exhaust: a study of time kinetics using induced sputum. Eur Respir J 2000; 15:1046-1051
400
Franciosi LG, Page CP, Celli BR, Cazzola M, et al. Markers of exacerbation severity in chronic
obstructive pulmonary disease. Respir Res 2006; 7:74-88
401
Spencer S, Calverley PM, Burge PS, Jones PW. Impact of preventing exacerbations on deterioration of
health status in COPD. Eur Respir J 2004; 23:698-702
61
3.9 Management of COPD
Management of COPD includes effective accurate diagnosis and treatment of COPD and its
complications and comorbidities (Disease Management), then training the patient and carers to
monitor and respond appropriately to changes in the condition (Chronic Disease Self
Management). Aspects of management have been reviewed in the GOLD Guidelines402,403, and
COPD-X404,405 but are summarized below and in Table 3.5.
TABLE 3.5.
COPD-X MANAGEMENT PLAN FOR COPD406,407
Management
Principle
Broad Description of Management Actions
C
Confirm diagnosis and severity (requires symptoms & spirometry).
Check for complications and comorbidities.
Optimise patient function, with safe effective medications.
Encourage and assist activity & good nutrition.
Provide oxygen if hypoxaemic.
Prevent deterioration:
Stop smoking.
Pulmonary rehabilitation.
Develop shared-care Action Plan
O
P
D
X
Exacerbation treatment plan:
early diagnosis & treatment
systemic corticosteroids
effective antibiotics if bacterial infection
oxygenate if hypoxaemic
ventilate if ventilatory failure
Only selected references are provided for important studies or meta-analyses. The
pharmacotherapy aspects have been well-reviewed recently408, and overall management has also
been reviewed409. Staging using GOLD (www.goldcopd.org), NICE (www.nice.org.uk) or
COPD-X (www.copdx.org.au) guidelines can help to guide therapy (Table 3.6).
402
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
403
Rabe KF, Hurd S, Anzueto A, et al. Global Strategy for the diagnosis, management, and prevention of
COPD: GOLD executive summary. Am J Respir Crit Care Med 2007; 176:532-555
404
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
405
Abramson MJ, Crockett AJ, Frith PA, McDonald CF. COPDX: an update of guidelines for the
management of chronic obstructive pulmonary disease with a review of recent evidence. Med J Aust 2006;
184:342-345
406
McKenzie DK, Frith PA, Burdon JG, Town GI. ibid
407
Abramson MJ, Crockett AJ, Frith PA, McDonald CF. ibid
408
Dransfield MT, Bailey WC. Maintenance pharmacotherapy of chronic obstructive pulmonary disease:
an evidence-based approach. Expert Opin Pharmacother 2005; 6:13-25
409
Sin DD, McAlister FA, Man SF, Anthonisen NR. Contemporary management of chronic obstructive
pulmonary disease: a scientific review. JAMA 2003; 290:2301-2312
62
TABLE 3.6.
COPD STAGES AS A GUIDE TO TREATMENT
Stage
All stages
I: Mild
II:
Moderate
III: Severe
IV: Very
Severe
Add treatments (high levels of
evidence of efficacy and
safety)
Avoid risk factors (especially
smoking)
Symptom relief (as-needed
bronchodilators)
Regular long-acting
anticholinergic and/or long
acting beta agonist.
Pulmonary rehabilitation
Inhaled corticosteroids
Treat complications
Recommended treatment
Add treatments (good evidence
Consider in individual cases
of efficacy and safety)
(low evidence across
populations)
Influenza vaccination.
Pneumococcal vaccination
Maintain regular activity
Avoid unhelpful treatments and
drug interactions
Inhaled corticosteroids
Long-term home oxygen if
respiratory failure
Consider oral theophylline
Consider LVRS / transplant
Consider home ventilation
Because of its many impacts on patients and their families, COPD can be considered a multisystem bio-psychosocial disorder, making a multidisciplinary approach to care entirely logical.
Symptom control can to some extent be improved with shorter-acting bronchodilators. A
systematic review found only four trials meeting Cochrane criteria, and confirmed efficacy in
exacerbations of COPD, but found no difference between ipratropium and beta-agonist410.
In people with severe airflow limitation reduction in exacerbations can be achieved, exercise
capacity can be improved, and decline in quality of life can be slowed, without significant risk, by
long-acting beta-agonists411,412 (LABA).
The long-acting anticholinergic drug, tiotropium, reduces hyperinflation, reduces exacerbations,
increases exercise endurance, reduces dyspnoea, improves quality of life413, and enhances effects
of pulmonary rehabilitation414,415,416,417,418,419. A meta-analysis has confirmed these findings420.
410
McCrory DC, Brown CD. Anticholinergic bronchodilators versus beta2-sympathomimetic agents for
acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2004; Issue 4
411
Jones PW, Wilson K, Sondhi S. Cost-effectiveness of salmeterol in patients with chronic obstructive
pulmonary disease: an economic evaluation. Respir Med 2003; 97:20-26
412
Sovani MP, Whale CI, Tattersfield AE. A benefit-risk assessment of inhaled long-acting beta2-agonists
in the management of obstructive pulmonary disease. Drug Safety 2004; 27:689-715
413
Barr RG, Bourbeau J, Camargo CA, Ram FSF. Tiotropium for stable chronic obstructive pulmonary
disease: a meta-analysis. Thorax 2006; 61:854-862
414
Niewoehner DE, Rice K, Cote C, Paulson D, et al. Prevention of exacerbations of chronic obstructive
pulmonary disease with tiotropium, a once-daily inhaled anticholinergic bronchodilator. A randomised
trial. Annals Intern Med 2005; 143:317-326
415
Casaburi R, Mahler DA, Jones PW, et al. A long-term evaluation of once-daily inhaled tiotropium in
chronic obstructive pulmonary disease. Eur Respir J 2002; 19:217-224
416
Vincken W, van Noord JA, Greethorst APM, et al. Improved health outcomes in patients with COPD
during 1 yr’s treatment with tiotropium. Eur Respir J 2004; 23:832-840
417
Celli B, ZuWallack R, Wang S, et al. Improvements in resting inspiratory capacity and hyperinflation
with tiotropium in COPD with increased static lung volumes. Chest 2003; 124:1743-1748
418
O’Donnell DE, Fluge T, Gerken F, Hamilton A, et al. Effects of tiotropium on lung hyperinflation,
dyspnoea and exercise tolerance in COPD. Eur Respir J 2004; 23:832-840
419
Casaburi R, Kukafka D, Cooper CB, Witek TJ, Kesten S. Improvement in exercise tolerance with the
combination of tiotropium and pulmonary rehabilitation in patients with COPD. Chest 2005; 127:809-817
63
There may be significant additional benefit from combining use of tiotropium and a
LABA421,422,423, although tiotropium may have better overall efficacy424.
Despite its inflammatory nature, COPD has long been considered poorly responsive to inhaled
corticosteroids (ICS). Recent research, however, has shown potential for ICS425, especially in
combination with LABA, not only to slow decline in quality of life and reduce exacerbations and
hospitalisations but perhaps also reduce mortality426,427,428,429,430,431,432,433,. A systematic review
found six relevant RCTs with 4,118 patients treated with ICS-LABA (pooling of both available
combinations was used), and determined there were consistent benefits in quality of life,
symptoms and rates of exacerbations in comparison with placebo, but little evidence relating to
comparison with the mono-components434. Post hoc analysis from the TORCH trial435, and a
nested case control study from a cohort of COPD patients (n=175,906)436 suggest an increased
risk of pneumonia in people with COPD receiving inhaled corticosteroids (with or without
420
Barr RG, Bourbeau J, Camargo CA, Ram FSF. Tiotropium for stable chronic obstructive pulmonary
disease: a meta-analysis. Thorax 2006; ………………..
421
Cazzola M, Centanni S, Santus P, Verga M, et al. The functional impact of adding salmeterol and
tiotropium in patients with stable COPD. Respir Med 2004; 98:1214-1221
422
Cazzola M, Di Marco F, Santus P, Boveri B, et al. The pharmacodynamic effects of single inhaled doses
of formoterol, tiotropium and their combination in patients with COPD. Pulmon Pharmacol Therapeutics
2004; 17:35-39
423
Cazzola M, Noschese P, Salzillo A, De Giglio C, et al. Bronchodilator response to formoterol after
regular tiotropium or to tiotropium after regular formoterol in COPD patients. Respir Med 2005; 99:524528
424
Brusasco V, Hodder R, Miravitlles M, Korducki F, et al. Health outcomes following treatment for six
months with once daily tiotropium compared with twice daily salmeterol in patients with COPD. Thorax
2003; 58:399-404
425
Yang IA., Fong KM, Sim EHA et al. Inhaled corticosteroids for stable chronic obstructive pulmonary
disease. Cochrane Database Syst Re 2007, Issue 2. Art No: CD002991
426
Pauwels RA, Lofdahl CG, Laitinen LA, et al. Long-term treatment with inhaled budesonide in persons
with mild chronic obstructive pulmonary disease who continue smoking: European Respiratory Society
Study on Chronic Obstructive Pulmonary Disease. N Engl J Med 1999; 340:1948-1953
427
Burge PS, Calverley PMA, Jones PW, on behalf of the ISOLDE study investigators. Randomized,
double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic
obstructive pulmonary disease: the ISOLDE trial. Brit Med J 2000; 320:1297-1303
428
The Lung Health Study Research Group. Effects of inhaled triamcinolone on the decline in pulmonary
function in chronic obstructive pulmonary disease. N Engl J Med 2000; 343:1902-1909
429
Soriano JB, Kiri VA, Pride NB, Vestbo J. Inhaled corticosteroids with/without long-acting Гџ-agonists
reduce risk of rehositalization and death in COPD patients. Am J Respir Med 2003; 2:67-74
430
Sin DD, Wu L, Anderson JA, et al. Inhaled corticosteroids and mortality in chronic obstructive
pulmonary disease. Thorax 2005; 60:992-997
431
Macie C, Wooldrage K, Manfreda J, Anthonisen NR. Inhaled corticosteroids and mortality in COPD.
Chest 2006; 130:640-646
432
Calverley PMA, Anderson JA, Celli B, et al. Salmeterol and fluticasone propionate and survival in
chronic obstructive pulmonary disease. New Engl J Med 2007; 356:775-789
433
Macie C, Wooldrage K, Manfreda J, Anthonisen NR. Inhaled corticosteroids and mortality in COPD.
Chest 2006; 130:640-646
434
Nanini L, Cates CJ, Lasserson TJ, Poole P. Combined corticosteroid and longacting beta-agonist in one
inhaler for chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2004; Issue 4
435
Calverley PMA, Anderson JA, Celli B, et al. Salmeterol and fluticasone propionate and survival in
chronic obstructive pulmonary disease. New Engl J Med 2007; 356:775-789
436
Ernst P, Gonzalez AV, Brassard P, Suissa S. Inhaled corticosteroid use in chronic obstructive pulmonary
disease and the risk of hospitalization for pneumonia. Am J Respir Crit Care Med 2007; 176:162-166
64
additional drugs). Further definitive research addressing this possibility is indicated, but the
findings warrant clinical monitoring of all patients treated with ICS who have severe COPD.
Additional benefits may be found from adding tiotropium to combined ICS-LABA in severe
COPD (and deterioration after withdrawal of tiotropium)437, and a recent Canadian RCT has
confirmed additional effects on exacerbation rates (but not on lung function, quality of life or
exacerbation rates)438. Another small study (randomized, double blind double dummy three-way
cross-over) in COPD patients aged 40-80 and with FEV1 averaging 47.1% predicted
demonstrated greater lung function improvements, reduced hyperinflation and improved levels of
dyspnoea from combined tiotropium and salmeterol+fluticasone than with tiotropium alone and
the ICS-LABA439.
Supplemental oxygen in the home was found in two landmark controlled trials to improve
survival of patients with COPD who are significantly hypoxaemic, especially if there was either
polycythaemia or pulmonary hypertension440,441. The benefits were seen when the duration of
treatment was longer than 15 hours a day (with greater benefit from longer hours of
supplementation). Pulmonary haemodynamics have been shown to improve and stabilise in such
settings442.. More recent studies have not been so favourable when evaluating survival in those
with mild hypoxaemia443,444, or in severely hypoxaemic patients with multiple comorbidities445. In
prescribing home oxygen therapy, there are significant imperfections, however. Adherence to
recommendations based on evidence by the physician is not infrequently poor446,447,448, and
patients adhere to instructions poorly449,450. In particular smoking cessation is central, given the
437
Perng D-W, Wu C-C, Su K-C, et al. Additive benefits of tiotropium in COPD patients treated with longacting Гџ2 agonists and corticosteroids. Respirology 2006; 11:598-602
438
Aaron SD, Vandemheen KL, Fergusson D, Maltais F, et al. Tiotropium in combination with placebo,
salmeterol, or fluticasone-salmeterol for treatment of chronic obstructive pulmonary e. A randomized trial.
Annals Intern Med 2007; 146:545-555
439
Singh D, Brooks J, Hagan G, Cahn A, O’Connor BJ. Superiority of “triple” therapy with
salmeterol/fluticasone propionate and tiotropium bromide versus individual components in moderate to
severe COPD. Thorax 2008; 63:592-598
440
Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxaemic
chronic obstructive lung disease – a clinical trial. Annals Intern Med 1980; 93:391-398
441
Report of the Medical Research Council Working Party. Long-term domiciliary oxygen therapy in
chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981; i:681-686
442
Zielinski J, Tobiasz M, Hawrylkiewicz I, et al. Effects of long-term oxygen therapy on pulmonary
hemodynamics in COPD patients. A 6-year prospective study. Chest 1998; 113:65-70
443
Fletcher EC, Donner CF, Midgren B, Zielinski J, et al. Survival in COPD patients with a daytime PaO2
> 60 mm Hg and without nocturnal oxyhaemoglobin desaturation. Chest 1992; 101:649-655
444
Chaouat A, Weitzenblum E, Kessler R, Charpentier C, et al. A randomised trial of nocturnal oxygen
therapy in chronic obstructive pulmonary disease patients. Eur Respir J 1999; 14:1002-1008
445
Crockett AJ, Cranston JM, Moss JR, Alpers JH. Survival on long-term oxygen therapy in chronic
airflow limitation: from evidence to outcomes in the routine clinical setting. Intern Med J 2001; 31:448454
446
Morrison D, Skwarski K, MacNee W. Review of the prescription of domiciliary long term oxygen
therapy in Scotland. Thorax 1995; 50:1103-1105
447
Oba Y, Salzman GA, Willsie SK. Reevaluation of continuous oxygen therapy after initial prescription in
patients with chronic obstructive pulmonary disease. Respir Care 2000; 45:401-406
448
Cook DJ, Reeve BK, Griffith LE, et al. Multidisciplinary education for oxygen prescription: a
continuous quality improvement study. Arch Intern Med 1996; 156:1797-1802
449
Gorecka D, Gorselak K, Sliwinski P, et al. Effect of long term oxygen therapy on survival in patients
with chronic obstructive pulmonary disease with moderate hypoxaemia. Thorax 1997; 52:674-679
65
counter-productivity of ongoing smoking (eg on survival, and the potential for adverse interaction
between carbon monoxide and oxygen), as well the ever-present danger of fires sustained in the
presence of oxygen enrichment. PR professionals need to be alert to the fact that sometimes
patients revert to old habits, despite warnings and even agreements about these dangers. Ongoing
monitoring and reassessment are therefore warranted for people prescribed this therapy, and
targeted education for them and their carers is recommended (though supported by limited direct
evidence of efficacy for either approach)451,452.
The question of ambulatory or intermittent oxygen therapy is at present unresolved. Even a recent
systematic review453 has not answered the question, largely because they examined only RCTs,
and discovered only two such studies. An early trial in twenty patients supported the benefits of
ambulatory oxygen in COPD patients with secondary polycythaemia, in reducing the
polycythaemia, without adverse effects or intolerability454. Oxygen given for 5 minutes before or
for 5 minutes after a 6MWT (double-blind, random order design study) to people with moderate
to severe COPD who showed desaturation on a previous test of >4% had no appreciable benefit
in walk distance or breathlessness scores, and there was no difference between pre and postexercise gas treatment455. Exercise capacity may improve for mildly-hypoxaemic COPD patients
using portable oxygen at rest and during exercise testing456, activities457,458,459, and with exercise
training in PR460, as it appears to decrease dynamic hyperinflation461. A systematic review
examining the role of oxygen supplementation during exercise training found five RCTs
conducted in people with COPD without resting hypoxaemia462. Results were heterogeneous, and
no significant differences were found for functional exercise outcomes, maximal or sub-maximal
exercise performance or HRQoL. In interstitial lung disease the operational arguments around
450
Neri M, Melani AS, Miorelli AM, Zanchetta D, et al, for the Educational Study Group of the Italian
Association of Hospital Pulmonologists (AIPO). Long-term oxygen therapy in chronic respiratory failure: a
Multicenter Italian Study on Oxygen Therapy Adherence (MISOTA). Respir Med 2006; 100:795-806
451
Pelletier-Fleury N, Lanoe JL, Fleury B, Fardeau M. Cost effectiveness of two types of structure
delivering long term oxygen therapy at home. Rev D’Epidemiol Sante Publ 1997; 45:53-63
452
Pepin J-L, Barjhoux CE, Deschaux C, Brambilla C, on behalf of the ANTADIR Working Group on
Oxygen Therapy. Long-term oxygen therapy at home: compliance with medical prescription and effective
use of therapy. Chest 1996; 109:1144-1150
453
Ram FSF, Wedzicha JA. Ambulatory oxygen for chronic obstructive pulmonary disease. Cochrane
Database Syst Rev 2007, issue 4
454
Petty TL, Finigan MM. Clinical evaluation of prolonged ambulatory oxygen therapy in chronic airway
obstruction. Am J Med 1968; 45:242-252
455
Nandi K, Smith AA, Crawford A, et al. Oxygen supplementation before or after submaximal exercise in
patients with chronic obstructive pulmonary disease. Thorax 2003; 58:670-673
456
Alvisi V, Mirkovic T, Nesme P, et al. Acute effects of hyperoxia on dyspnea in hypoxemia patients with
chronic airway obstruction at rest. Chest 2003; 123:1038-1046
457
Jolly E, Di Boscio V, Aguirre L, Luna C, et al. Effects of supplemental oxygen during activity in
patients with advanced COPD without severe resting hypoxemia. Chest 2001; 120:437-443
458
Eaton T, Garrett J, Young P, Fergusson W, et al. Ambulatory oxygen improves quality of life of COPD
patients: a randomised controlled study. Eur Respir J 2002; 20:306-312
459
McDonald C, Blyth C, Lazarus M, Marschner I, Barter C. Exertional oxygen of limited benefit in
patients with chronic obstructive pulmonary disease and mild hypoxemia. Am J Respir Crit Care Med
1995; 152:1616-1619
460
Garrod R, Paul E, Wedzicha J. Supplemental oxygen during pulmonary rehabilitation in patients with
COPD with exercise desaturation. Thorax 2000; 55:539-543
461
O’Donnell D, D’Arsigny C, Webb K. Effects of hyperoxia on ventilatory limitation during exercise in
advanced chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001; 152:892-898
462
Nonoyama ML, Brooks D, Lasse Y, et al. Oxygen therapy during exercise training in chronic
obstructive pulmonary disease. Cochrane database Syst rev 2008, Issue 1
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oxygen supplementation are different. Patients with interstitial disease who desaturate from
normoxia to hypoxaemia during exertion have shorter survivals463. More research is warranted on
the benefits (including survival, exercise endurance, and quality of life) and costs (both financial
and personal inconvenience) of ambulatory oxygen therapy. Australian and New Zealand
recommendations for domiciliary oxygen therapy have been updated in 2005, with
acknowledgement that the evidence base needs strengthening464.
Oral corticosteroids should be avoided in the long term because they are not effective and they
have important deleterious adverse effects. However they are indicated in acute exacerbations as
they speed recovery465.
Recurrent inflammation from infections may be prevented by vaccinations, notably against
influenza, but perhaps also against Pneumococcus. If antibiotics are used promptly for symptoms
of bacterial infection of the lower respiratory tract recovery is quicker, and inflammatory damage
is therefore probably reduced. Infections are the main cause of exacerbations of COPD, and these
often lead to hospitalization, further reduce quality of life, increase mortality, All these aspects of
medication use, and the equipments available to administer them, should feature in education of
the patient and carers.
Weight loss arising from the catabolic state of advanced disease predicts rapid progression466,467.
Good nutrition should therefore be maintained before this stage is reached, and this can also
maintain a sense of well-being and prevent loss of lean muscle mass468,469. There is suggestive
evidence that diet high in some flavonoids with anti-inflammatory and anti-oxidant effects
reduces symptoms and protects against decline in lung function470. Excessive weight increases
work of breathing, and makes coexisting hypoventilation or upper airway obstruction during
sleep more likely, so attainment and maintenance of ideal weight should be encouraged. This is
more important when supporting people who are quitting smoking, as weight gain during the first
year of cessation resulted in small but significant reductions in operating lung volumes in the
US/Canadian Lung Health Study involving 5,346 individuals, especially deleterious in men471.
Sleep-disordered breathing is relatively common, is related to excess weight, impairs
ventilation during sleep, may contribute to poor control of cardiovascular disease, and needs
treatment with assisted ventilation (CPAP).
463
Lama VN, Flaherty KR, Toews GB, Colby TV, et al. Prognostic value of desaturation during a 6-minute
walk test in idiopathic interstitial pneumonia. Am J Respir Crit Care Med 2003; 168:1084-1090
464
McDonald CF, Crockett AJ, Young IH. Adult domiciliary oxygen therapy. Position statement of the
Thoracic Society of Australia and New Zealand. Med J Aust 2005; 182:621-626
465
Wood-Baker R, Walters EH, Gibson P. Oral corticosteroids for acute exacerbations of chronic
obstructive pulmonary disease. Cochrane Database Syst Rev 2004; Issue 4
466
Wilson DO, Rogers RM, Wright EC, Anthonisen NR. Body weight in chronic obstructive pulmonary
disease. The National Institutes of Health Intermittent Positive-Pressure Breathing Trial. Am Rev Respir Dis
1989; 139:1435-1438
467
Gray-Donald K, Gibbons L, Shapiro SH, Macklem PT, Martin JG. Nutritional status and mortality in
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1996; 153:961-966
468
Schols AM, Slangen J, Volovics L, Wouters EF. Weight loss is a reversible factor in the prognosis of
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157:1791-1797
469
Rogers RM, Donahoe M, Costantino J. Physiologic effects of oral supplemental feeding in malnourished
patients with chronic obstructive pulmonary disease. A randomized control study. Am Rev Respir Dis 1992;
146:1511-1517
470
Tabak C, Arts ICW, Smit HA, et al. Chronic obstructive pulmonary disease and intake of catechins,
flavonols, and flavones. The MORGEN Study. Am J Respir Crit Care Med 2001; 164:61-64
471
Wise RA, Enright PL, Connett JE, Anthonisen NR, et al. Effect of weight gain on pulmonary function
after smoking cessation in the Lung Health Study. Am J Respir Crit Care Med 1998; 157:866-872
67
Moderate and severe COPD often result in a plethora of psychosocial difficulties, and these
should be addressed in the management plan. Distinction between mood and psychopathological
disease can be difficult. Dyspnoea is a distressing symptom, and inactivity leading to social
withdrawal and loss of role can cause patients and carers to be disheartened. Depressive
symptoms are common in chronic respiratory diseases (COPD and asthma)472. Depression and
anxiety with or without panic disorder are moderately frequent in COPD, and could potentially be
helped by pharmacotherapy or cognitive behaviour therapy. A large Canadian random population
health survey (n=36,984) used the World Mental Health Composite International Diagnostic
Interview, a technique more likely to identify true psychiatric diagnoses than do mental health
screening questionnaires; with a 77% response rate. Subjects were asked to select from an
extensive list what chronic medical conditions had been diagnosed. This evaluation found 4,448
people reported one or more respiratory illnesses, and these people had high prevalence rates of
major depression, panic disorder and substance dependence473. The links are greater with more
severe disease, and appear to be independent of therapies (including long-term oxygen
therapy)474. A systematic review in 1999475 found only four case-control studies out of ten studies
with otherwise satisfactory methodological design, and rates of depression varied widely,
between 7% and 42%. Anxiety in COPD has been largely ignored, although the prevalence of
476,477,478
, and it appears to contribute significant
anxiety in COPD may be between 8% and 67%
479,480
. The impact of comorbid depression on
risk of hospitalisation for patients with COPD
outcomes in COPD patients has been examined in a prospective cohort of 376 consecutive
patients hospitalised for exacerbations of COPD, and depressive symptoms were independently
associated with higher rates of re-hospitalisation, persistent smoking, worse symptoms, and
higher mortality rates481. In a later cross-sectional study of 109 oxygen-dependent patients with
severe COPD, 57% had significant depressive symptoms, with 18% being severely clinically
depressed482. Other research suggests that depression is not uncommon in stable patients with
472
Moussas G, Tselebis A, Karkanias A, et al. A comparative study of anxiety and depression in patients
with bronchial asthma, chronic obstructive pulmonary disease and tuberculosis in a general hospital of
chest diseases. Annals Gen Psychiatry 2008; 7:7-10
473
Patten SB, Williams JVA. Chronic obstructive lung disease and prevalence of mood, anxiety, and
substance-abuse disorders in a large population sample. Psychosomatics 2007; 48:496-501
474
Lewis KE, Annandale JA, Sykes RN, et al. Prevalence of anxiety and depression in patients with severe
COPD: Similar high levels with and without LTOT. COPD: J COPD 2007; 4:305-312
475
van Ede L, Yzermans CJ, Brouwer HJ. Prevalence of depression in patients with chronic obstructive
pulmonary disease: A systematic review. Thorax 1999; 54:688-692
476
Rose c, Wallace l, Dickson R, Ayres J, et al. The most effective psychologically-based treatments to
reduce anxiety and panic in patients with chronic obstructive pulmonary disease (COPD): a systematic
review. Pat Educ Counsel 2002; 47:311-318
477
Brenes GA. Anxiety and chronic pulmonary disease: Prevalence, impact and treatment. Psychosom Med
2003; 65:963-970
478
Dowson CA, Kuijer RG, Mulder RT. Anxiety and self-management behaviour in chronic obstructive
pulmonary disease: what has been learned? Chronic Respir Dis 2004; 1:213-220
479
Yohannes AM, Baldwin RC, Commolly MJ. Depression and anxiety in elderly outpatients with chronic
obstructive pulmonary disease: prevalence and validation of the BASDEC screening questionnaire. Internat
J Geriatric Psych 2000; 15:1090-1096
480
Gudmunsson G, Gislason T, Janson C, Lindberg E, et al. Risk factors for rehospitalisation in COPD:
role of health status, anxiety and depression. Eur Respir J 2005; 26:414-4192005
481
Ng T-P, Niti M, Tan W-C, et al. Depressive symptoms and chronic obstructive pulmonary disease.
Effect on mortality, hospital readmission, symptoms burden, functional status, and quality of life. Arch
Intern Med 2007; 167:60-67
482
Lacasse Y, Rousseau L, Maltais F. Prevalence of depressive symptoms and depression in patients with
severe oxygen-dependent chronic obstructive pulmonary disease. J Cardiopulm Rehabil 2001; 21:80-86
68
severe COPD483,484,485, especially among smokers486. In addition, depression and anxiety occurred
with quite high frequency in New Zealand patients hospitalized with COPD487. The overall
interaction between mood disorders and COPD has also been reviewed488.
Given these findings, use of anti-depressants or anxiolytics, or non-pharmacological treatments
ought to be considered. The response rates in older depressed patients who are treated with
antidepressants are thought to be as high as 50 to 60%489. A systematic review has found that
antidepressants were more effective than placebo in older inpatients and outpatients with
depression490. Evidence for the benefit of antidepressant therapy for older COPD patients with
491,492
depression is incomplete
. Anxiety is often a significant problem in people with COPD and
SSRIs are beneficial in reducing anxiety as well as depression493. Weight gain may occur
particularly with longer term therapy, and this may be a useful “adverse effect” in underweight
COPD patients494. Mirtazipine may also be considered for underweight patients with agitated
depression, provided therapy is commenced at a low dose and the patient is monitored carefully
for respiratory depression. Buspirone has been found clinically to be a useful anxiolytics without
respiratory suppression495.
Cognitive behaviour therapy (CBT) is a psychotherapeutic modality that aims to identify
anxiety-provoking automatic thoughts and change both these negative thoughts and the
underlying beliefs through behavioural tasks like diary-keeping, with validity-testing of beliefs
between sessions and skills training in sessions496. There is good evidence supporting CBT in a
483
Kostianev S, Mitrev I, Hodgev V, et al. Dyspnoea, depression and anxiety in patients with chronic
obstructive pulmonary disease. Bulg Med J 2001; 9:23-25
484
Yohannes AM, Roomi J, Baldwin RC, Connolly MJ. Depression in elderly outpatients with disabling
chronic obstructive pulmonary disease. Age & Ageing 1998; 27:155-160
485
van Manen JG, Bindels PJ, Ilzermans CJ, van der Zee JS, et al. Prevalence of comorbidity in patients
with a chronic airway obstruction and controls over the age of 40. J Clin Epidemiol 2001; 54:287-293
486
Kostianev S, Mitrev I, Hodgev V, et al. ibid
487
Dowson C, Paing R, Barraclough R, Town I, et al. The use of the Hospital Anxiety and Depression
Scale (HADS) in patients with chronic obstructive pulmonary disease: A pilot study. New Zealand Med J
2001; 114:447-449
488
Clary GL, Palmer SM, Doraiswamy PM. Mood disorders and chronic obstructive pulmonary disease:
Current research and future needs. Current Psychiat Reports 2002; 4:213-221
489
Schneider LS, Olin TJ. Efficacy of acute treatment of geriatric depression. Internat J Geriatric Psych
1995; 7(Suppl 7):7-25
490
Wilson K, Mottram P, Sivanranthan A, Nightingale A. Antidepressants versus placebo for the depressed
elderly. Cochrane Database Syst Rev 2001; Issue 1
491
Yohannes AM, Connolly MJ, Baldwin RC. 2001. A feasibility of antidepressant drug therapy in
depressed elderly patients with chronic obstructive pulmonary disease. Internat J Geriatric Psych 2001;
16:451-454
492
Lacasse Y, Beaudoin L, Rousseau L, Maltais F. Randomized trial of paroxetine in end-stage COPD.
Monaldi Arch Chest Dis 2004; 61: 140–147.
493
Rossie, S, Vitry A, Hurley E, Abbott F, Eds. Australian Medicines Handbook. Adelaide: Australian
Medicine Handbook Pty Ltd 2006.
494
Masand PS, Gupta S. Long-term side effects of newer-generation antidepressants: SSRIs, venlafaxine,
nefazodone, bupropion and mirtazipine. Ann Clin Psych 2002; 14:175-182
495
Alderman CP, Frith PA, Ben-Tovim DI. Buspirone for the treatment of anxiety in patients with chronic
obstructive airways disease. J Clin Psychopharm 1996; 16: 410-411
496
Hunot V, Churchill R, Silva de Lima M, Teixeira V. Psychological therapies for generalised anxiety
disorder. Cochrane Database Syst Rev 2006; Issue 4
69
497,498,499
variety of syndromes and settings
studied.
, but its utility in COPD has not been systematically
Loss of exercise capacity with breathlessness can lead to fear of activity, panic, loss of confidence
and depression. The consequent lack of activity can contribute to loss of muscle mass and
strength. Encouragement therefore needs to be given to increase activities and formal exercise
strength and endurance training has strong evidence for its efficacy.
MANAGEMENT OF COPD
KEY POINTS
1)
Stages of severity based on symptoms and lung function can be
used to guide therapy.
2)
Evidence-based management of COPD includes facilitating
early diagnosis, rating severity, detecting complications, reducing
risk factors, guiding drug therapy, maintaining activity, referring
for rehabilitation, providing oxygenation, and support.
3)
Smoking cessation slows COPD progression.
4)
The progressive natural history of COPD and its multi-system
effects require careful lifetime monitoring.
5)
An ongoing disease management system is required, linking
primary care and other care sectors, and involving a shared-care
approach with the patient.
6)
Support and education can be provided through Support
Groups, Pulmonary Rehabilitation, and Outreach programs.
7)
Attention should be given to palliative care and end-of-life
issues in later Stages of the condition.
497
O’Kearney RT, Anstey KJ, von Sanden C. Behavioural and cognitive behavioural therapy for obsessive
compulsive disorder in children and adolescents. Cochrane Database Syst Rev 2006; Issue 4
498
James A, Soler A, Weatherall R. Cognitive behavioural therapy for anxiety disorders in children and
adolescents. Cochrane Database Syst Rev 2006; Issue 4
499
Price JR, Couper J. Cognitive behaviour therapy for chronic fatigue syndrome in adults. Cochrane
Database Syst Rev 1998; Issue 4
70
4. PULMONARY
REHABILITATION
4.1 Introduction
Rehabilitation within Lung Disease
Management
Evidence-based guidelines for management of COPD, and more specifically for Pulmonary
Rehabilitation, first emerged in the 1990s. American Thoracic Society (ATS) Official Statement
on “Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary
Disease” (1995)500, and British Thoracic Society (BTS) “BTS Guidelines for the Management of
Chronic Obstructive Pulmonary Disease” (1997)501 emerged each with discussion on Pulmonary
Rehabilitation (PR). Based on extensive references they concluded that PR should be an integral
part of the management of patients with moderate to severe disability. By PR each Society was
referring to a multi-disciplinary program aimed at patient wellbeing and functional status. The
BTS did not give any detail of the components of PR, while the ATS Guidelines did.
Management of COPD
There has been a reasonably comprehensive cover of this topic in the previous Section. Many
components of COPD management are integral parts of PR, however, and for this reason the
topic is presented in summary format, and specific aspects that are of most relevance to PR are
detailed below. Web-based documents are also available for more in-depth discussion.
International (�GOLD’) COPD Guidelines were published after wide consultation and extensive
literature searches502. They originally listed four components of management:
• Assess and monitor disease
• Reduce risk factors
• Manage stable COPD
• Manage exacerbations
In Australia and New Zealand the TSANZ and ALF co-developed COPD-X (see previous
Section), a four-step management guideline503,504. New guidelines aimed at primary care have
500
American Thoracic Society Official Statement. Standards for the Diagnosis and Care of Patients with
Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med 1995; 152:S77-S120
501
COPD Guidelines Group, BTS. BTS Guidelines for the Management of Chronic Obstructive Pulmonary
Disease. Thorax 1997; 52 (Suppl 5):S4-S27
502
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
503
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003; 178
(Suppl):S1-S40
71
also recently been published in the UK505. Recommendations are thoroughly evidence based in
both, covering diagnosis, preventative approaches, and managing stable patients, exacerbations
and progression of disease through optimum treatment and self-management plans.
Assess and Monitor Disease
It is beyond the scope of this document to present further discussion on this aspect. It is, however,
the responsibility of the physicians involved in PR programs to assess each patient in sufficient
detail so that all respiratory diagnoses, complications of the disease and its treatment, and
concurrent conditions are accurately diagnosed. PR physicians should initiate investigations
and/or referrals for opinion if other conditions are suspected and treatment is found to be
inadequate. In doing so, the physician should integrate actions with the relevant primary care
doctor, and fully inform others involved in the patient’s care.
Reduce Risk Factors
There is a range of risk factors for the development and progression of COPD, as detailed
previously. All pulmonary rehabilitation workers should be actively involved in promoting
healthy living choices as part of their commitment to primary and secondary prevention, and
helping their patients achieve a lifestyle that minimizes ongoing exposure to risk.
Tobacco Smoking
Smoking cessation is the leading risk reduction strategy, as it is the single most effective and
cost-effective disease modifying treatment506. As smoking is the major risk factor for
development and progression of COPD, and a frequent trigger for asthma, intensive efforts in
primary and secondary prevention are indicated. This implies a multi-facetted approach that
includes patient education, overall review of lifestyle, pharmacological and behavioral support,
and ongoing review. Several guidelines for smoking cessation have been published in recent
years, including those from the US Public Health Service507,508, the UK509, and Australia510, as
well as many books, pamphlets and programs that provide support and information for people
wanting to quit. Brief (e.g. 3 minutes) intervention by the physician can be effective511. The “Five
504
Abramson MJ, Crockett AJ, Frith PA, McDonald CF. COPDX: an update of guidelines for the
management of chronic obstructive pulmonary disease with a review of recent evidence. Med J Aust 2006;
184:342-345
505
The National Collaborating Centre for Chronic Conditions. Chronic obstructive pulmonary disease.
National clinical guidelines on management of chronic obstructive pulmonary disease in adults in primary
and secondary care. Thorax 2004; 59 (Suppl I):1-232
506
Rabe KF, Hurd S, Anzueto A, et al. Global Strategy for the diagnosis, management, and prevention of
COPD: GOLD executive summary. Am J Respir Crit Care Med 2007; 176:532-555
507
The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium
Representatives. A clinical practice guideline for treating tobacco use and dependence. JAMA 2000;
283:244-254
508
American Medical Association. Guidelines for the diagnosis and treatment of nicotine dependence: how
to help patients stop smoking. Washington, DC: American Medical Association; 1994
509
West R, McNeill A, Raw M. Smoking cessation guidelines for health professionals: an update. Thorax
2000; 55:987-999
510
National Preventive & Community Medicine Committee of the Royal Australian College of General
Practitioners. Putting Prevention into Practice. Guidelines for the implementation of prevention in the
general practice setting. RACGP, Melbourne; 1998
511
Wilson DH, Wakefield MA, Steven ID, Rohrsheim RA, et al. “Sick of Smoking”: evaluation of a
targeted minimal smoking cessation intervention in general practice. Med J Aust 1990; 152:518-521
72
A’s” are principles common to most interventions512 (see Box). The full evidence base has been
reviewed for all recommendations in the UK guidelines, and in several other keynote
publications513,514,515,516.
THE FIVE A’s QUIT STRATEGY
517
ASK – current and past smoking at each visit
ASSESS – nicotine addiction, habits, and readiness to quit
ADVISE – health effects, how to quit, withdrawal, supports
ASSIST – quit tools (drugs, counselling and support)
ARRANGE – regular follow-up to ensure abstinence
BENEFITS OF SMOKING CESSATION
Smoking cessation has many benefits. Some are outside the scope of this Manual, but include
reduction of risk for development or progression of cardiovascular disease and peripheral arterial
disease, and progressive reduction in risk for development of several cancers, especially those of
the respiratory tract. The benefits related to respiratory disease are also multiple. These were the
subject of a recent systematic review518. Spanish and Polish studies have shown that spirometry
screening can result in increased uncovering of airflow limitation in symptomatic smokers, and
that this discovery of early COPD can enable many smokers to quit519.
512
The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium
Representatives. A clinical practice guideline for treating tobacco use and dependence. JAMA 2000;
283:244-254
513
Glynn TJ, Manley MW, Pechacek TF. Physician-initiated smoking cessation program: the National
Cancer Institute trials. Prog Clin Biol Res 1990; 339:11-25
514
Lancaster T, Stead L, Silagy C, Sowden A. Effectiveness of interventions to help people stop smoking:
findings from the Cochrane Library. Brit Med J 2000; 321:355-358
515
van der Meer RM, Wagena EJ, Ostelo RWJG, Jacobs JE, van Schayck CP. Smoking cessation for
chronic obstructive pulmonary disease. (Cochrane Review). The Cochrane Library, Oxford.: Update
Software 2003; Issue 3
516
National Institute for Clinical Excellence. Guidance on the use of Nicotine Replacement Therapy (NRT)
and buproprion for smoking cessation. NICE Technology Appraisal Guidance No 39, London. National
Institute for Clinical Excellence; 2002
517
The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium
Representatives. A clinical practice guideline for treating tobacco use and dependence. JAMA 2000;
283:244-254
518
Willemse BWM, Postma DS, Timens W, ten Hacken NHT. The impact of smoking cessation on
respiratory symptoms, lung function, airway hyperresponsiveness and inflammation. Eur Respir J 2004;
23:464-476
519
Clotet J, Gomez-Arbones X, Ciria C, Albalad JM. Spirometry is a good method for detecting and
monitoring chronic obstructive pulmonary disease in high-risk smokers in primary health care. Arch
Bronconeum 2004; 40:155-159
73
Respiratory symptoms are differentially responsive to smoking cessation. In cross-sectional
studies, background cough, sputum production and wheezing are all lower in prevalence in exsmokers than in current smokers. Prevalence of cough is reported in 5 to 21% of ex-smokers but
10 to 40% in current smokers. Sputum production is reported in 5 to 30% of ex-smokers and 10
to 40% of current smokers. The reported range for prevalence of wheezing is 1 to 19% in exsmokers and between 7 and 32% in continuing smokers. However, the sensation of dyspnoea
appears to be less responsive, with prevalence rates between 2 and 41% in both smoker and
former smokers. Further, the prevalence rates of all these respiratory symptoms remain higher in
ex-smokers than in people who have never smoked.
In longitudinal studies it has been shown that some symptoms are less likely to develop in people
who quit smoking than in those who persist. Development of cough or sputum production, for
example, was seen in 21% of smokers who quit compared to 29% of persisting smokers520.
Cough, sputum production and wheezing all decrease within a few months of smoking cessation.
Indeed, the prevalence of cough and wheeze decreased to that in non-smokers521. Sputum
persisted, albeit at a reduced rate, and dyspnoea was not altered in this study522. Dyspnoea may
decrease slightly523, or not at all524. Alternatively weight gain following smoking cessation may
contribute to an increase in dyspnoea with exertion, possibly related to restriction of operating
lung volumes with the weight gain525.
In people with established COPD, there are few longitudinal data relating to change in respiratory
symptoms following smoking cessation. Development of symptoms is greater in continuing
smokers than in those who persistently quit526,527. A disappearance of chronic cough has been
described528, while the large Lung Health Study confirmed over 80% reduction in chronic cough,
chronic sputum, day and night wheeze and dyspnoea after 5 years of smoking cessation529, mostly
in the first year of quitting. Sustained quitters were later found to have lower rates of lower
respiratory tract infections than continuing smokers530.
520
Krzyzanowski M, Robbins DR, Lebowitz MD. Smoking cessation and changes in respiratory symptoms
in two populations followed for 13 years. Int J Epidemiol 1993; 22:666-673
521
Comstock GW, Brownlow WJ, Stone RW, Sartwell PE. Cigarette smoking and changes in respiratory
findings. Arch Environ Health 1970; 21:50-57
522
Tashkin DP, Clark VA, Coulson AH, et al. The UCLA population studies of chronic obstructive
respiratory disease. VIII. Effects of smoking cessation on lung function: a prospective study of a free-living
population. Am Rev Respir Dis 1984; 130:707-715
523
Peterson DI, Lonergan LH, Hardinge MG. Smoking and pulmonary function. Arch Environ Health
1968; 16:215-218
524
Israel RH, Ossip-Klein DJ, Poe RH, et al. Bronchial provocation tests before and after cessation of
smoking. Respiration 1998; 54:247-254
525
Wise RA, Enright PL, Connett JE, Anthonisen NR, et al. Effect of weight gain on pulmonary function
after smoking cessation in the Lung Health Study. Am J Respir Crit Care Med 1998; 157:866-872
526
Kanner RE, Connet JE, Williams DE, Buist AS. Effects of randomized assignment to a smoking
cessation intervention and changes in smoking habits on respiratory symptoms in smokers with early
chronic obstructive pulmonary disease: the Lung Health Study. Am J Med 1999; 106:410-416
527
Pride NB. Smoking cessation: effects on symptoms, spirometry and future trends in COPD. Thorax
2001; 56 (Suppl 2):117-110
528
Friedman GD, Siegelaub AB. Changes after quitting cigarette smoking. Circulation 1980; 61:716-723
529
Anthonisen N, Connett J, Kiley J, Altose M, et al. Effects of smoking intervention and the use of an
inhaled anticholinergic bronchodilator on the rate of decline of FEV1. JAMA 1994; 272:1497-1505
530
Kanner RE, Anthonisen NR, Connett JE for the Lung Health Study Research Group. Lower respiratory
illnesses promote FEV1 decline in current smokers but not ex-smokers with mild chronic obstructive
pulmonary disease. Results from the Lung Health Study. Am J Respir Crit Care Med 2001; 164:358-364
74
Several studies slower deterioration of lung function in people who successfully quit smoking
compared with those who persist. Cross-sectional531,532,533,534 and longitudinal studies, including
the Framingham Study and others, have confirmed the reduced rate of loss of lung function over
time in successful quitters compared to those who continue to smoke, and some data have
suggested that the rate of lung function decline reaches the normal rate by two years after
quitting535,536,537,538,539,540. Recent analysis from the Lung Health Study has demonstrated FEV1
decline rates averaging 27 mls per year in sustained quitters, while continuing smokers
deteriorated by an average of 60 ml a year541. At 11 years, FEV1 values had declined to less than
60% of predicted normal in 38% of continuing smokers and in 10% of sustained quitters.
In people with COPD the decline in lung function that accelerates with age and further increases
with smoking, is faster in people with higher cumulative smoking consumption and with actual
numbers smoked542, and appears to be greater again in people with bronchial hyperresponsiveness543. In the Lung Health Study, people who continued to smoke had higher rates of
lower respiratory infections and a combination of lower respiratory infections and sustained
smoking accelerated further the decline in lung function544. Smoking is associated with an
increase in airway responsiveness545, generally thought to be due to the airway inflammation
531
Higgenbottam T, Clark TJ, Shipley MJ, Rose G. Lung function and symptoms of cigarette smokers
related to tar yield and number of cigarettes smoked. Lancet 1980; 1:409-411
532
Nemery B, Moavero NE, Brasseur L, Stanescu DC. Changes in lung function after smoking cessation:
an assessment from a cross-sectional survey. Am Rev Respir Dis 1982; 125:122-124
533
Dockery DW, Speizer FE, Ferris BG, Ware JH, et al. Cumulative and reversible effects of lifetime
smoking on simple tests of lung function in adults. Am Rev Respir Dis 1988; 137:286-292
534
Sorlie P, Lakatos E, Kannel WB, Celli B. Influence of cigarette smoking on lung function at baseline
and at follow-up in 14 years: the Framingham Study. J Chronic Dis 1987; 40:849-856
535
Bosse R, Sparrow D, Rose CL, Weiss ST. Longitudinal effect of age and smoking cessation on
pulmonary function. Am Rev Respir Dis 1981; 123:378-381
536
Townsend MC, DuChene AG, Morgan J, Browner WS. Pulmonary function in relation to cigarette
smoking and smoking cessation. MRFIT Research Group. Prev Med 1991; 20:621-637
537
Tashkin DP, Clark VA, Coulson AH, et al. The UCLA population studies of chronic obstructive
respiratory disease. VIII. Effects of smoking cessation on lung function: a prospective study of a free-living
population. Am Rev Respir Dis 1984; 130:707-715
538
Xu X, Dockery DW, Ware JH, Speizer FE, Ferris BG. Effects of cigarette smoking on rate of loss of
pulmonary function in adults: a longitudinal assessment. Am Rev Respir Dis 1992; 146:1345-1348
539
Burchfield CM, Marcus EB, Curb JD, et al. Effects of smoking and smoking cessation on longitudinal
decline in lung function. Am J Respir Crit Care Med 1995; 151:1778-1785
540
Pelkonen M, Notkola IL, Tukianen H, Tervahauta M, et al. Smoking cessation, decline in pulmonary
function and total mortality: a 30 year follow up study among the Finnish cohorts of the Seven Countries
Study. Thorax 2001; 56:703-707
541
Anthonisen NR, Connett JE, Murray RP, for the Lung Health Study Research Group. Smoking and lung
function of Lung Health Study participants after 11 years. Am J Respir Crit Care Med 2002; 166:675-679
542
Scanlon PD, Connett JE, Waller LA, Altose MD, et al. Smoking cessation and lung function in mild-tomoderate chronic obstructive pulmonary disease. The Lung Health Study. Am J Respir Crit Care Med
2000; 161:381-390
543
Postma DS, de Vries K, Koeter GH, Sleiter HJ. Independent influence of reversibility of air-flow
obstruction and non-specific hyperreactivity on the long-term course of lung function in chronic air-flow
obstruction. Am Rev Respir Dis 1986; 134:276-280
544
Kanner RE, Anthonisen NR, Connett JE for the Lung Health Study Research Group. Lower respiratory
illnesses promote FEV1 decline in current smokers but not ex-smokers with mild chronic obstructive
pulmonary disease. Results from the Lung Health Study. Am J Respir Crit Care Med 2001; 164:358-364
545
Yan K, Salome CM, Woolcock AJ. Prevalence and nature of bronchial hyperresponsiveness in subjects
with chronic obstructive pulmonary disease. Am Rev Respir Dis 1985; 132:25-29
75
induced by smoking546,547,548,549, as well as an epi-phenomenon of altered airway geography (that
is, reduced airway calibre)550,551,552. An interaction between airway reactivity and smoking has
been described in the Lung Health Study, such that those with baseline increased methacholine
reactivity had steeper declines in lung function than in smokers without hyperreactivity553, and
this was unrelated to baseline FEV1. The same benefits in lung function and symptoms as seen in
normal smokers from quitting have been demonstrated in several cross-sectional554 and
prospective studies of people with COPD555,556,557 (see Diagram 4.1).
FIGURE 4.1
DECLINE IN LUNG FUNCTION558
546
Van Schoor J, Joos GF, Pauwels RA. Indirect bronchial hyperresponsiveness in asthma: mechanisms,
pharmacology and implications for clinical research. Eur Respir J 2000; 16:514-533
547
Pesci A, Rossi GA, Bertorelli G, Aufiero A, et al. Mast cells in the airway lumen and bronchial mucosa
of patients with chronic bronchitis. Am J Respir Crit Care Med 1994; 149:1311-1316
548
Hong JL, Rodger IW, Lee LY. Cigarette smoke-induced bronchoconstriction: cholinergic mechanisms,
tachykinins, and cyclooxygenase products. J Appl Physiol 1995; 78:2260-2266
549
Renkema TE, Kerstjens HA, Schouten JP, Vonk JM, et al. The importance of serum IgE for level and
longitudinal change in airways hyperresponsiveness in COPD. Clin Exper Allergy 1998; 28:1210-1218
550
Ramsdale EH, Morris MM, Roberts RS, Hargreave FE. Bronchial responsiveness to methacholine in
chronic bronchitis: relationship to airflow obstruction and cold air responsiveness. Thorax 1984; 39:912918
551
Finkelstein R, Ma HD, Ghezzo H, Whittaker K, et al. Morphometry of small airways in smokers and in
relationship to emphysema type and hyperresponsiveness. Am J Respir Crit Care Med 1995; 152:267-276
552
Koyama H, Nishimura K, Ikeda A, Sakai N, et al. Influence of baseline airway calibre and pulmonary
emphysema on bronchial responsiveness in patients with chronic obstructive pulmonary disease. Respir
Med 1996; 90:323-328
553
Tashkin DP, Altose MD, Connett JE, Kanner RE, et al. Methacholine reactivity predicts changes in lung
function over time in smokers with early chronic obstructive lung disease. Am J Respir Crit Care Med
1996; 153:1802-1811
554
Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J 1977; 1:1645-1648
555
Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smoking intervention and the use of an inhaled
anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA 1994;
272:1497-1505
556
Murray RP, Anthonisen NR, Connett JE, et al. Effects of multiple attempts to quit smoking and relapses
to smoking on pulmonary function. Lung Health Study Research Group. J Clin Epidemiol 1998; 51:13171326
557
Anthonisen NR, Connett JE, Murray RP. Smoking and lung function of Lung Health Study participants
after 11 years. Am J Respir Crit Care Med 2002; 166:675-679
558
Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J 1977; 1:1645-1648
76
Improvements in airway hyperresponsiveness have also been described in people with COPD
who quit smoking. These improvements include tests of both direct and indirect
hyperresponsiveness. Tests of direct specific receptor-activated smooth muscle constriction by
inhaled histamine or methacholine deteriorated less in sustained quitters than in continuing
smokers in the longitudinal Lung Health Study559, though no such differences were seen in crosssectional studies of smoking and ex-smoking populations560. Tests of indirect smooth muscle
effects of adenosine 5’-monophosphate (AMP) through activation of inflammatory cells and/or
neural pathways have been shown to be less active in a cross-sectional study of ex-smokers than
current smokers561, and confirmed in an uncontrolled longitudinal study of 14 smokers with
COPD who sustained quitting for one year562. This latter study also showed reduced direct
responsiveness, but showed no relationship between these changes and induced sputum markers
of airway inflammation. The changes in symptoms and lung function with smoking, and their
improvement after successful quitting, are not as consistently matched by pathological changes in
the lungs563. Goblet cell hyperplasia, even in non-COPD patients undergoing lung resection, is
slightly less in ex-smokers than current smokers564. This benefit is more marked in those with
COPD565. Some changes with smoking and after cessation, in COPD and without, have been
described in expression of bronchial inflammatory mediators566, and inflammatory markers in the
blood and sputum appear lower in ex-smokers than in continuing smokers567,568,569,570,571. That is,
in people with COPD, although some airway inflammation appears to persist even after smoking
cessation572, reductions observed in alveolar, serum and sputum markers suggest the tissues
effects ameliorate with time573,574,575,576,577.
559
Wise RA, Kanner RE, Lindgren P, et al. The effect of smoking intervention and an inhaled
bronchodilator on airways reactivity in COPD: the Lung Health Study. Chest 2003; 124:449-458
560
Postma DS, Renkema TE, Noordhoek JA, Faber H, et al. Association between non-specific bronchial
hyperreactivity and superoxide anion production by polymorphonuclear leukocytes in chronic airflow
obstruction. Am Rev Respir Dis 1988; 137:57-61
561
Oosterhoff Y, de Jong JW, Jansen MA, et al. Airway responsiveness to adenosine 5’-monophosphate in
chronic obstructive pulmonary disease is determined by smoking. Am Rev Respir Dis 1993; 147:553-558
562
Willemse BWM, ten Hacken NHT, Rurgers B, Lesman-Leegte IGAT, et al. Smoking cessation
improves both direct and indirect airway hyperresponsiveness in COPD. Eur Respir J 2004; 24:391-396
563
Wright JL, Hobson JE, Wiggs B, et al. Airway inflammation and peribronchiolar attachments in the
lungs of nonsmokers, current and ex-smokers. Lung 1988; 166:277-286
564
Mullen JB, Wright JL, Wiggs BR, et al. Structure of central airways in current smokers and ex-smokers
with and without mucus hypersecretion: relationship to lung function. Thorax 1987; 42:843-848
565
Wright JL, Lawson LM, Pare PD, Wiggs BJ, et al. Morphology of peripheral airways in current smokers
and ex-smokers. Am Rev Respir Dis 1983; 127:474-477
566
Skold CM, Hed J, Eklund A. Smoking cessation rapidly reduces cell recovery in bronchoalveolar lavage
fluid, while alveolar macrophage fluorescence remains high. Chest 1992; 101:989-995
567
Capelli A, Di Stefano A, Gnemmi I, et al. Increased MCP-1 and MIP-1ОІ in bronchoalveolar lavage fluid
of chronic bronchitics. Eur Respir J 1999; 14:160-165
568
Skold CM, Blashke E, Eklund A. Transient increases in albumin and hyaluronan in bronchoalveolar
lavage fluid after quitting smoking: possible signs of reparative mechanisms. Respir Med 1996; 90:523-529
569
Skold CM, Forslid J, Eklund A, Hed J. Metabolic activity in human alveolar macrophages increases
after cessation of smoking. Inflammation 1993; 17:345-352
570
de Jong JW, Belt-Gritter B, Koeter GH, Postma DS. Peripheral blood lymphocyte cell subsets in
subjects with chronic obstructive pulmonary disease: association with smoking, IgE and lung function.
Respir Med 1997; 91:67-76
571
Dentener MA, Creutzberg EC, Schols AM, et al. Systemic anti-inflammatory mediators in COPD:
increase in soluble interleukin 1 receptor II during treatment of exacerbations. Thorax 2001; 56:721-726
572
Pesci A, Rossi GA, Bertorelli G, Aufiero A, et al. Mast cells in the airway lumen and bronchial mucosa
of patients with chronic bronchitis. Am J Respir Crit Care Med 1994; 149:1311-1316
573
Jensen EJ, Pedersen B, Schmidt E, Venge P, Dahl R. Serum eosinophilic cationic protein and lactoferrin
related to smoking history and lung function. Eur Respir J 1994; 7:927-933
77
Finally, analyses from the Lung Health Study Research Group have demonstrated increases in
hospitalisation rates and higher 5-year mortality in continuing smokers than in sustained
quitters578. The Group has confirmed the reduction in all-cause mortality from quitting in the most
recent 14.5-year follow-up analysis of the original 5,887 smoking cohort (aged 35-60 years at
origin)579. A Finnish cohort study followed for 30 years (enrolling all eligible males aged 40-59
years in 1959) provides further powerful data580, confirming the other studies. Lung function
predicted all-cause mortality after adjustment for cardiovascular risk factors; smoking cessation
improved mortality (mainly due to reduced cardiovascular deaths, seen within the first five years
of quitting); deaths attributed to COPD or lung cancer did not decline, however, probably due to
the lack of benefit from smoking cessation described in those with more severe COPD581,582.
Manage Stable COPD
In managing stable disease, the elements of education, pharmacologic treatment, and nonpharmacologic treatments are defined within GOLD583, COPD-X584,585, and NICE586 guidelines
for the management of COPD. In each case, education is considered important, though each paper
acknowledges that studies of effectiveness for education alone in COPD are rare. Specific aspects
of education are effective, including smoking cessation, explanation of optimum inhaled
medications and apparatus, as well as oxygen use and self-management. Rehabilitation is the first
aspect in non-pharmacologic treatment in these guidelines, and they all emphasise that careful
evaluation has identified a range of clear benefits. The components of PR are addressed –
574
Scott DA, Stapleton JA, Wilson RF, et al. Dramatic decline in circulating intercellular adhesion
molecule-1 concentration on quitting tobacco smoking. Blood Cells Molec Dis 2000; 26:255-258
575
Scott DA, Stapleton JA, Palmer RM, et al. Plasma concentrations of reputed tumor-associated CD44
isoforms (v5 and v6) in smokers are dose related and decline on smoking cessation. Cancer Epidemiol
Biomarkers Prev 2000; 9:1211-1214
576
Rennard SJ, Daughton D, Fujita J, et al. Short-term smoking reduction is associated with reduction in
measures of lower respiratory tract inflammation in heavy smokers. Eur Respir J 1990; 3:752-759
577
Vernooy JH, Kucukaycan M, Jacobs JA, et al. Local and systemic inflammation in patients with chronic
obstructive pulmonary disease: soluble tumor necrosis factor receptors are increased in sputum. Am J
Respir Crit Care Med 2002; 166:1218-1224
578
Anthonisen NR, Connett JE, Enright PL, Manfred J, and the Lung Health Study Research Group.
Hospitalizations and mortality in the Lung Health Study. Am J Respir Crit Care Med 2002; 166:33-339
579
Anthonisen NR, Skeans MA, Wise RA, et al. The effects of a smoking cessation intervention on 14.5year mortality. A randomized clinical trial. Ann Intern Med 2005; 142:233-239
580
Pelkonen M, Tikainen H, Tervahauta M, et al. Pulmonary function, smoking cessation and 30 year
mortality in middle aged Finnish men. Thorax 2000; 55:746-750
581
Burrows B, Earle RH. Predictors of survival in patients with chronic airways obstruction. Am Rev Respir
Dis 1969; 99:865-871
582
Anthonisen NR, Wright EC, Hodgkin JE, et al. Prognosis in chronic obstructive pulmonary disease. Am
Rev Respir Dis 1986; 133:14-20
583
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
584
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
585
Abramson MJ, Crockett AJ, Frith PA, McDonald CF. COPDX: an update of guidelines for the
management of chronic obstructive pulmonary disease with a review of recent evidence. Med J Aust 2006;
184:342-345
586
The National Collaborating Centre for Chronic Conditions. Chronic obstructive pulmonary disease.
National clinical guidelines on management of chronic obstructive pulmonary disease in adults in primary
and secondary care. Thorax 2004; 59 (Suppl I):1-232
78
specifically exercise training, nutrition counseling, and education. Depression, anxiety and panic
are acknowledged as issues, but the GOLD document does not discuss this further, while the
NICE document provides extensive analytical discussion.
Manage Acute Exacerbations
Through the PR program and in collaboration with the patient and primary care doctor, each
patient should be trained to self-manage, by monitoring symptoms and signs, and to responding
quickly with an agreed safe and effective treatment strategy if symptoms, signs or lung function
worsen. Clear guidelines should be shared with and agreed by the health care team so consistent
evidence-based but individualized treatments are given. The aim is to allow the patient to avoid
whenever possible the need for life-disrupting admission to hospital.
Relevant recent systematic reviews relating to exacerbation management include non-invasive
ventilation587, methylxanthines588, hospital at home care589, bronchodilator treatment590, and
antibiotics591. The management of exacerbations is outlined in GOLD (www.goldcopd.org)592 and
NICE (www.nice.org.uk)593, and is specifically presented in the COPD-X management guide
(www.copdx.org.au)594,595. A useful summary of mechanisms and management for COPD
exacerbations was published in 2003596.
Goals of Pulmonary Rehabilitation
•
•
•
•
to improve adherence to recommended therapies
to reduce frequency and severity of symptoms
to improve mood and motivation
to reduce dependency and increase involvement with friends and family
587
Ram FSF, Pico J, Lightowler J, Wedzicha JA. Non-invasive positive pressure ventilation for treatment
of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database
Syst Rev 2006: Issue 3
588
Barr RG, Rowe BH, Camargo CA. Methylxanthines for exacerbations of chronic obstructive pulmonary
disease. Cochrane Database Syst Rev 2006; Issue 3
589
Ram FSF, Wedzicha JA, Wright J, Greenstone M. Hospital at home for acute exacerbations of chronic
obstructive pulmonary disease. Cochrane Database Syst Rev 2006; Issue 3
590
McCrory DC, Brown CD. Anticholinergic bronchodilators versus beta2-sympathomimetic agents for
acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2006; Issue 3
591
Ram FSF, Rodriguez-Roisin R, Granados-Navarette A, et al. Antibiotics for exacerbations of chronic
obstructive pulmonary disease. Cochrane Database Syst Rev 2006; Issue 3
592
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
593
The National Collaborating Centre for Chronic Conditions. Chronic obstructive pulmonary disease.
National clinical guidelines on management of chronic obstructive pulmonary disease in adults in primary
and secondary care. Thorax 2004; 59 (Suppl I):1-232
594
McKenzie DK, Frith PA, Burdon JG, Town GI. The COPDX Plan: Australian and New Zealand
Guidelines for the management of Chronic Obstructive Pulmonary Disease 2003. Med J Aust 2003;
178(Suppl):S1-S40
595
Abramson MJ, Crockett AJ, Frith PA, McDonald CF. COPDX: an update of guidelines for the
management of chronic obstructive pulmonary disease with a review of recent evidence. Med J Aust 2006;
184:342-345
596
Exacerbations in COPD and Asthma. Mechanisms and Medicines. Lund, Sweden. Proc Am Thorac Soc
2004; 1:71-145
79
• to enhance participation in therapeutic decisions by building selfmanagement capacity
• to increase participation in and enjoyment of everyday activities
• to improve quality of life
• to reduce health care burden for patients, families and communities
FIGURE 4.2
ENJOYMENT OF EVERYDAY ACTIVITIES SHOULD BE POSSIBLE FOR MOST PEOPLE
WITH COPD
Benefits of Pulmonary Rehabilitation
In brief, benefits documented in randomised controlled trials and other research include:
• better exercise capacity and endurance
• better health-related quality of life / health status
• return to work
• reduced perceived level of breathlessness
• increased knowledge about respiratory disease and management
• reduced hospitalisation rate and days per admission
• reduced healthcare costs
• enhanced mood, reduced anxiety, reduced depression
• improved self-efficacy
• enhanced ability to perform activities of daily living
• improved strength
• extended survival
80
Components of Pulmonary Rehabilitation
British Thoracic Society Statement on Pulmonary Rehabilitation597 lists five components:
• Education
• Physical training
• Psychological support and behavioural intervention
• Physiotherapy and relaxation exercises with energy conservation
• Nutrition.
European598,599, American600 and joint601 guidelines for pulmonary rehabilitation include similar
categories, and add recommendations for four main outcome assessments:
• Dyspnoea
• Quality of life
• Health-care utilisation
• Survival
All these elements of PR programs and the evidence supporting their use are considered in detail
in the following text.
4.2 Overviews of COPD and Rehabilitation
Evidence review 1971-1994
In thirty-one studies on COPD rehabilitation from the 1971-1994 medical literature
systematically reviewed by P Frith and P Walker there were 1,536 subjects assessed. The range of
sample sizes per study was 10 to 182. The average age was 59.8 years, though three studies did
not report the ages of their subjects. The range of mean ages varied between 50 and 67, and most
studies elected only to assess men. Average FEV1 ranged between 0.78L and 1.38L. This
probably represents values between 20% and 55% of predicted for age and height, though only
ten studies reported FEV1 as a percentage of the predicted value. Only 5 studies reported resting
pO2 or gas transfer. We came to several conclusions at that time.
1.
The utility of lung function tests to assess outcome from exercise training programs is
limited. A range of laboratory measures of exercise performance is widely used to assess the
degree of physical limitation (disablement) in COPD. One or more exercise evaluations were
used in 12 studies. The most common combination was a maximal test of exercise capacity
(usually incremental cycle ergometry) and a functional measure such as a six or twelve minute
walk test. Of the studies that elected to only use one measure, incremental treadmill exercise
performance was the most commonly used (five).
597
British Thoracic Society Standards of Care Subcommittee on Pulmonary Rehabilitation. Pulmonary
rehabilitation. Thorax 2001; 56:827-834
598
Donner CF, Decramer M. Pulmonary rehabilitation. Eur Resp Soc Monogr 2000; 13
599
Donner CF, Muir JF. Selection criteria and programmes for pulmonary rehabilitation in COPD patients.
Eur Respir J 1997; 10:744-757
600
AACVPR/ACCP Pulmonary Rehabilitation Guidelines Panel. Pulmonary Rehabilitation. Joint
ACCP/AACVPR evidence-based guidelines. Chest 1997; 112:1363-1396
601
Nici L, Donner C, Wouters E, ZuWallack R, et al, on behalf of the ATS/ERS Pulmonary Rehabilitation
Writing Committee. American Thoracic Society/European Respiratory Society Statement on Pulmonary
Rehabilitation. Am J Respir Crit Care Med 2006; 173:1390-1413
81
2.
Eight of the 31 studies reviewed either did not measure any aspect of HRQoL, or did not
use reliable and valid measuring instruments, or reported HRQoL without defining the
instruments. The remaining studies used a variety of measures to assess HRQoL. Most used
generic questionnaires to measure physical and emotional function. In only 3 studies reviewed in
1995 was a disease specific questionnaire used – the Chronic Respiratory Disease Questionnaire
(CRDQ).
3.
The nature of rehabilitation programs is highly variable. Seven of the studies published
to 1994 were inpatient based, and ranged in duration (2 to 8 weeks) and exercise intensity (15
minutes once a day to 4 to 5 hours a day seven days a week). Programs offered different exercise
regimens, from walking, stair climbing, swimming, and cycle ergometer to upper body
conditioning. Some programs offered pulmonary education, while others did not. The remaining
studies were outpatient based, and also ranged considerably in duration (4 weeks to 6 months),
exercise intensity (5 minutes to 3 hours a day), and exercise type (upper body, inspiratory muscle
training, stair climbing, cycle ergometry, upper body conditioning).
4.
The timing of outcome measurements varies in the reviewed trials. Short-term outcome
measures, within the first 3-4 months, were most usually taken, only evaluating subjects directly
after the intervention programs. Only ten of the studies assessed longer-term outcomes greater
than 5 months after program implementation and withdrawal.
5.
The methods of patient selection, randomisation and control also vary. Fifteen of the 31
studies reviewed did not have a control group. Thirteen of these showed a statistically significant
increase in some measure of exercise capacity. Curiously, neither of the remaining two used
exercise testing to evaluate the outcome of an exercise program. The interpretations of outcomes
from such uncontrolled studies must be treated with caution. Motivation, attentional influences,
practice effect due to greater familiarity with test protocols, and familiarity with staff may
alleviate anxiety and so may have contributed significantly to improvements in exercise
performance and quality of life.
6.
The specifics of rehabilitation components were also different. Eight of the 15
uncontrolled studies of exercise training incorporated other modalities of pulmonary
rehabilitation (eg. breathing re-training, education) into their programs. Four did not assess any
changes in HRQoL. Two alluded to subjective changes and two gave anecdotal accounts of
improvements in quality of life. The remaining studies found reduced affective distress, sensation
of dyspnoea, disability scores and fatigue, and improved well-being, self-efficacy and mastery.
Sixteen controlled studies were identified.
Nine of these used a control group that did not receive any form of intervention.
The training programs in these 9 studies ranged in duration from 3 to 12 weeks, though the
duration was not made clear in 2 studies. None of these 9 studies was able to demonstrate
improvement in maximal exercise capacity when compared to the control group. Statistically
significant (small) changes were seen in exercise endurance, shortness of breath and well-being
compared to control groups. Three of the 9 controlled studies used well-validated health status
questionnaires. Cockroft found improvements in both groups’ affective states, although changes
were not statistically significant602. Both Goldstein603 and Wijkstra604 found improvements in
experimental group’s mastery, dyspnoea and emotional function, but not fatigue (CRDQ).
602
Cockcroft AE, Saunders MJ, Berry G. Randomised controlled trial of rehabilitation in chronic
respiratory disability. Thorax 1981; 36:200-203
82
Seven studies used a treatment control group.
Lustig605 randomly allocated 45 adult patients with COPD to either an experimental group (which
received 15 to 20 pulmonary rehabilitation treatments), or one of two control groups (which
received either psychotherapy or no treatment). The outcome measure was Minnesota
Multiphasic Personality Inventory (MMPI), and Mann-Whitney U tests were used for analysis
(not appropriate for analysing change scores). The experimental group showed improvement
compared to the no treatment group, but not compared to the psychotherapy group. This suggests
a significant effect of therapy regardless of its modality, and may indicate an attentional effect.
Degre606 compared the effects of exercise training in 11 COPD subjects with a breathing exercise
program in 5 COPD subjects (not randomly assigned). This study did not measure quality of life.
Physiological data from pulmonary function tests and tests of exercise capacity were measured.
No mention was made of the statistical procedures. The only significant change post-intervention
was in resting partial oxygen tension in the exercise group, from 76mmHg to 82mmHg (of little
clinical significance). No correction was made for the multiple comparisons of the data (30 in
all), which, along with the small sample size, greatly reduces the power of the study.
Kaplan607 used three experimental groups: a behaviour modification group, a cognitive
modification group, and a cognitive-behaviour modification group, compared to an attention
control group (which spent six sessions completing psychological questionnaires and a variety of
neuropsychological tasks, requiring little interaction). There was no placebo treatment for
controls, and no treatment expectancy was induced. The paper gave no information regarding the
number of subjects in each group or the dropout rates. The three experimental groups improved
significantly compared to the control group in health status, exercise tolerance, exercise capacity,
and self-efficacy, but there was no significant difference between the three experimental groups.
Jones608 randomly allocated severe COPD subjects to one of two training programs: a physical
exercise (n=8) or a resistive training (n=7); or to placebo training (n=6). There were significant
improvements in all three groups’ maximal exercise capacity and global mood but no significant
changes in lung function, respiratory symptoms or 12MWD. The small sample size and multiple
comparisons made using paired and un-paired t-tests limit the statistical power. The results
suggest that improvements in HRQoL were independent of the type of program used.
Toshima609 studied over 100 adults with COPD, randomised into rehabilitation group (twelve 4hour sessions in 8 weeks) or “education control” group (four 2-hour biweekly meetings at which
603
Goldstein RS, Gort EH, Stubbing D, Avendano MA, Guyatt GH. Randomised controlled trial of
respiratory rehabilitation. Lancet 1994; 344:1394-1397
604
Wijkstra PJ, van Altena R, Kraan J, Otten V, et al. Quality of life in patients with chronic obstructive
pulmonary disease improves after rehabilitation at home. Eur Respir J 1994; 7:269-273
605
Lustig FM, Haas A, Castillo R. Clinical and rehabilitation regime in patients with chronic obstructive
pulmonary disease. Arch Phys Med Rehabil 1972; 53:315-322
606
Degre S, Sergysels R, Messin R, Vandermoten P, et al. Hemodynamic responses to physical training in
patients with chronic lung disease. Am Rev Respir Dis 1974; 110:395-402
607
Kaplan RM, Atkins CJ, Reinsch S. Specific efficacy expectations mediate exercise compliance in
patients with COPD. Health Psychol 1984; 3:223-242
608
Jones DT, Thomson RJ, Sears MR. Physical exercise and resistive breathing training in severe chronic
airways obstruction: Are they effective? Eur J Respir Dis 1985; 67:159-165
609
Toshima MT, Kaplan RM, Ries AL. Experimental evaluation of rehabilitation in chronic obstructive
pulmonary disease: short-term effects on exercise endurance and health status. Health Pyschol 1990;
9:237-252
83
they were given information regarding respiratory disease). There were attentional differences
between the two groups - the rehabilitation group had 48 hours of rehabilitation and the control
group had only 8 hours of education. The educational content of the two programs differed. The
rehabilitation group had more lectures than controls, individual instruction and practice with
respiratory care techniques, group meetings with a psychiatrist, and an exercise training program
with behavioural techniques. Repeated measures analysis of variance showed a substantial
increase in exercise performance and self-efficacy for walking for the rehabilitation group that
lasted over six months, but little improvement in the control group. There were no differences
between the groups’ quality of well-being or depression scores over time.
Lake610 randomly allocated COPD patients into either a control group (n=7), or upper limb
training (n=5), lower limb (n=7) or combined (receiving both upper and lower limb training)
(n=7) exercise groups. There was a significant training effect in the combined and lower limb
groups’ walk distances and the upper limb and combined groups’ arm ergometry. Significant
improvement was seen in the self-efficacy scores of the combined group, but no significant
changes in the other groups. The study was limited by small sample size, non-validated selfefficacy scale and sub-optimal statistics.
Weiner611 compared patients randomly assigned to either inspiratory muscle training with general
exercise reconditioning (group A, n=12), or general exercise reconditioning with placebo (group
B, n=12) or control (no training) (group C, n=12). After six months group A showed a significant
improvement in walking distance compared to the other groups, and both groups A and B showed
significant improvement in exercise endurance on a cycle ergometer compared to group C. No
measures of quality of life were used, and small samples limit generalisation.
Evidence reviews 1995-2001, 2001-2004,
2006 and 2008
There has been a profusion of new research into many aspects of PR (and the underlying
pathophysiologic bases of impairment, disability and handicap in chronic lung diseases). J
Cranston, A Crockett and P Frith systematically reviewed the available literature on pulmonary
rehabilitation and related topics published between 1995 and 2001. P Frith and J Cranston
updated this review with papers published between 2001 and 2004. Since then P Frith has
continuously updated review of the literature, with assistance from P Cafarella, J Duffy, J Alison,
L Spencer, S Jenkins, and members of the Pulmonary Rehabilitation Toolkit Steering Committee.
A number of additional controlled trials were identified, and there was greater use of diseasespecific health status measures. More attention had been given to other modalities than exercise
training, and to comprehensive pulmonary rehabilitation, as these are reviewed under
Comprehensive Pulmonary Rehabilitation, using the meta-analyses by Lacasse612,613 and
subsequent randomised controlled trials. Our extensive literature updated in 2001 was conducted
using:
610
Lake FR, Henderson K, Briffa T, Openshaw J, Musk AW. Upper-limb and lower-limb exercise training
in patients with chronic airflow obstruction. Chest 1990; 97:1077-1082
611
Weiner P, Azgard Y, Ganam R. Inspiratory muscle training combined with general exercise
reconditioning in patients with COPD. Chest 1992; 102:1351-1356
612
Lacasse Y, Wong E, Guyatt GH, King D, et al. Meta-analysis of respiratory rehabilitation in chronic
obstructive pulmonary disease. Lancet 1996; 348:1115-1119
613
Lacasse Y, Brosseau L, Milne S, Martin S, et al. Pulmonary rehabilitation for chronic obstructive
pulmonary disease. Cochrane Database Syst Rev 2006 Issue 2. CD003793
84
1. Gatewayв„ў, a Web-based system from the US National Library of Medicine, which includes
MEDLINE/PubMed, OLDMEDLINE, LOCATORplus, MEDLINEplus, DIRLINE, AIDS
Meetings, Health Services Research Meetings, Space Life Sciences Meetings, and HSRProj.a
GATEWAY search.
2. The OVIDTM database “Evidence Based Medicine”, which searches the Cochrane Database,
Best Evidence and DARE (Database of Reviews of Effectiveness).
3. The search engine “GOOGLE” was used to search the World-Wide Web.
The GOOGLE search without setting year limits yielded 12,800 hits for “standards + pulmonary
rehabilitation”, 5,520 hits for “standards + cardiopulmonary rehabilitation”, 20,100 hits for
“standards + cardiac rehabilitation”, and 4,140 hits for “pulmonary rehabilitation Australia”.
Using “Gateway”, with the terms “COPD AND pulmonary rehabilitation”, 1,280 citations were
found. Using terms “meta-analysis AND pulmonary rehabilitation” produced six meta473,
analyses614,615,616,617,618 and four systematic overviews 619,620,621. Cambach’s “research synthesis”
provided a true meta-analysis of non-randomised and randomised controlled trials of pulmonary
rehabilitation programs. Lacasse reviewed outcomes without a true meta-analysis. The remaining
papers reviewed systematically components of pulmonary rehabilitation – psychoeducational
care, physical therapy, ventilatory muscle training, nutrition, walk tests as outcomes, and an
overview of all components.
Using the OVID database with the terms “((COPD OR COAD OR COLD) AND pulmonary
rehabilitation).mp” with no year limits identified ten citations.
When the search was limited to 1998-2001, to discover publications not included in systematic
reviews cited above, 401citations were found, of which 363 were journal citations. Using
“Review AND pulmonary rehabilitation AND (COPD OR COAD OR COLD OR CAL)” with
limits set for 1998-2001 yielded 99 journal citations. With the terms “(randomized OR
randomised) AND (trial OR study) AND pulmonary rehabilitation AND COPD” 66 journal
citations were identified. The meta-analyses identified did not include a further 32 randomised
controlled trials identified in the 1998-2001 search strategy. These studies, the meta-analyses
(with their component trials), and the expert panel statements (US, UK, and international
guidelines of COPD management, and US, European and UK guidelines for pulmonary
614
Smith K. Respiratory muscle training in chronic airflow limitation: a meta-analysis. Am Rev Respir Dis
1992; 145:533-539
615
Devine EC, Pearcy J. Meta-analysis of the effects of psychoeducational care in adults with chronic
obstructive pulmonary disease. Patient Educ Couns 1996; 29:167-178
616
Cambach W, Wagenaar RC, Koelman TW, et al. The long-term effects of pulmonary rehabilitation in
patients with asthma and chronic obstructive pulmonary disease: a research synthesis. Arch Phys Med
Rehabil 1999; 80:103-111
617
Jones AP, Rowe BH. Bronchopulmonary hygiene physical therapy for bronchiectasis and chronic
obstructive pulmonary disease: a systematic review. Heart & Lung 2000; 29:125-135
618
Ferreira IM, Brooks D, Lacasse Y, Goldstein RS. Nutritional support for individuals with COPD: a
meta-analysis. Chest 2000; 117:672-678
619
Lacasse Y, Guyatt GH, Goldstein RS. The components of a respiratory rehabilitation program: a
systematic overview. Chest 1997 111:1077-1088
620
Lacasse Y, Goldstein RS. Overview of respiratory rehabilitation in chronic obstructive pulmonary
disease. Monaldi Arch Chest Dis 1999; 54:163-167
621
Solway S, Brooks D, Lacasse Y, Thomas S. A qualitative systematic overview of the measurement
properties of functional walk tests in the cardiopulmonary domain. Chest 2001; 119:256-270
85
rehabilitation) form the basis for the critical review presented below. Additional papers of
relevance to specific observations or recommendations are referenced.
A similar search methodology was repeated in September 2004, to update the above findings, and
has been updated progressively since. More nutrition and mental health papers have been
reviewed, and specific searches relating to mental health, self-management, as well as effects on
and roles of informal caregivers have been added.
Peripheral muscle impairments
In healthy individuals there is a large reserve of muscle metabolic capacity in skeletal muscles622.
Respiratory muscle demand in healthy subjects can compromise peripheral muscle blood flow623,
and the metabolic reserve enhanced by 100% oxygen breathing624, or other methods to reduce
work of breathing625. Peripheral muscle impairments is thought to exist in COPD as part of the
systemic illness626, and contribute to weakness, poor exercise tolerance, fatigue and reduced
endurance627,628,629,630,631,632. This has important consequences on patients’ ability to perform daily
activities633, and therefore impairs HRQoL634. The matter appears to be a circular one, in that
deconditioning due to inactivity associated with severe effort-induced dyspnoea is a major
determinant of impaired skeletal muscle function of lower limbs, with oxidative stress and
nutrition playing modulatory roles635. Objective measurements of muscle fatigue using
electromyograms (EMG) during sustained isometric contraction of quadriceps muscle has shown
622
Richardson RS, Knight DR, Poole DC, Kurdack SS, et al. Determinants of maximal exercise VO2
during single leg knee extensor exercise in humans. Am J Physiol 1995; 268:H1453-H1461
623
Richardson RS, Poole DC, Knight DR, Kurdack SS, et al. High muscle blood flow in man: is maximal
O2 extraction compromised? J Appl Physiol 1993; 75:1911-1916
624
Knight DR, Schaffartzik W, Poole DC, Hogan MC, et al. Hyperoxia increases leg maximal oxygen
uptake. J Appl Physiol 1993; 75:2586-2594
625
Harms CA, Babcock MA, McClaran SR, Pegelow DF, et al. Respiratory muscle work compromises leg
blood flow during maximal exercise. J Appl Physiol 1997; 82:1573-1583
626
Agusti AGN, Noguera A, Sauleda J, et al. Systemic effects of chronic obstructive pulmonary disease.
Eur Respir J 2003; 21:347-360
627
Hamilton AL, Killian KJ, Summers E, et al. Muscle strength, symptom intensity and exercise capacity
in patients with cardiorespiratory disorders. Am J Respir Crit Care Med 1995; 152:2021-2031
628
Gosselink R, Troosters T, Decramer M. Peripheral muscle weakness contributes to exercise limitation in
COPD. Am J Respir Crit Care Med 1996; 153;976-980
629
Maltais F, Simard AA, Simard C, et al. Oxidative capacity of the skeletal muscle and lactic acid kinetics
during exercise in normal subjects and patients with chronic obstructive pulmonary disease. Am J Respir
Crit Care Med 1996; 153:288-293
630
Bernard S, Leblanc P, Whittom F, et al. Peripheral muscle weakness in patients with chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 1998; 158:629-634
631
Couillard A, Maltais F, Saey D, et al. Exercise-induced quadriceps oxidative stress and peripheral
muscle dysfunction in patients with COPD. Am J Respir Crit Care Med 2003; 167:1664-1669
632
Mador MJ, Deniz O, Aggarwal A, et al. Quadriceps fatigability after single muscle exercise in patients
with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2003; 168:102-108
633
Serres I, Gautier V, Varray AL, Prefaut C. Impaired skeletal muscle endurance related to physical
inactivity and altered lung function in COPD patients. Chest 1998; 113:900-905
634
Yohannes AM, Roomi J, Waters K, Connolly MJ. Quality of life in elderly patients with COPD:
measurement and predictive factors. Respir Med 1998; 92:1231-1236
635
Gea J, Orozco-Levi M, Barreiro E, et al. Structural and functional changes in skeletal muscles of COPD
patients: The �compartments’ theory. Monaldi Arch Chest Dis 2001; 56:214-224
86
reduced muscle endurance due to reduced muscle oxidative capacity636, and fatigue637. Wagner
has summarised current state of knowledge about muscle impairment638.
Despite the evidence for skeletal muscle dysfunction in severe if not moderate COPD, metabolic
reserve may still be present if 100% oxygen can reduce ventilatory demand639. There are several
potential underlying causes – weakness of muscle through disuse atrophy and sometimes steroid
myopathy, poor tissue oxygen supply, abnormal neuromuscular conduction and abnormal muscle
energetics. Increasing evidence is being mounted to support the hypothesis that the latter is due
mainly to release of inflammatory cytokines640 and growth factors641 and imbalance in the muscle
redox systems642. Increased reliance of these muscles on anaerobic glycolysis therefore leads to
early lactic acid accumulation and premature muscle fatigue at lower work intensity643,644.
Importantly, the reduction in skeletal muscle endurance is poorly predicted by age, gender, level
of activity, severity of disease or muscle strength645,646, so each patient deserves careful
consideration of their muscle endurance and work capacity. Muscle loss includes both type I and
type II fibres in peripheral and ventilatory muscles. Ventilatory muscle function is further
impaired by altered chest wall shape from hyperinflation. This subject has been reviewed by
Mador and Bozkanat647.
It is worthwhile summarising current understanding of the oxidative stress in skeletal muscle in
people with COPD. Both weakness and fatigue may be due to inflammatory cytokines, such as
648,
tumour necrosis factor-alpha (TNF-α) 649. Animal studies suggest that disuse (�unloading’) of
636
Allaire J, Maltais F, Doyon J-F, Noel M, et al. Peripheral muscle endurance and the oxidative profile of
the quadriceps in patients with COPD. Thorax 2004; 59:673-678
637
Maltais F, Jobin J, Sullivan MJ, et al. Metabolic and hemodynamic responses of lower limb during
exercise in patients with COPD. J Appl Physiol 1998; 84:1573-1580
638
Wagner PD. Skeletal muscles in chronic obstructive pulmonary disease: Deconditioning, or myopathy?
Respirology 2006; 11:681-686
639
Richardson RS, Sheldon J, Poole DC, Hopkins SR, et al. Evidence of skeletal muscle metabolic reserve
during wholebody exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care
Med 1999; 159:881-885
640
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lower limbs provides another stimulus for oxidative stress650. In patients with COPD, heavy
exercise may induce abnormally high levels of oxidative stress, and this may actually be
preventable with oxygen therapy651. The abnormal levels of TNF-О± may be mediated by excess
reactive oxygen species652, possibly by releasing preformed TNF-О± directly from muscle
independent of induced RNA synthesis653, and this theory of direct release is supported by a lack
of gene down-regulation after training654. Further, TNF-О± levels consistently rise after moderateintensity endurance exercise in COPD patients without changes in levels of sTNFRs or IL-6. This
contrasts with the observation in healthy individuals that TNF-О± is increased with strenuous
exercise (such as after a marathon), but there is increased gene expression of interleukin-6 (IL6)655. Reactive oxygen species appear to target creatine kinase (CK) and carbonic anhydrase III
(CA-III) in peripheral muscles so that they are carbonylated, resulting in impaired CK function656.
Hypoxaemia appears to increase the oxidative stress by damaging lipids and proteins in vastus
lateralis muscles in patients with severe COPD, and evidenced by accumulation of lipofucsin in
the muscle fibres657, the latter confirmed in a case control study of COPD vs control vastus
lateralis muscles658.
The effects of hypoxaemia on muscle structure and function has been well summarised by
Fluck659. Diaphragmatic muscle fibres may be particularly susceptible to oxidative stress-induced
dysfunction according to case-control studies of diaphragmatic tissue from 6 patients with severe
COPD, 6 with moderate COPD and 7 control subjects without COPD, with negative correlations
between reactive carbonyl groups and airways obstruction660. Muscles seem to attempt autoregulation, and antioxidant activity in vastus lateralis muscles of 21 patients with severe COPD
and 12 healthy age-matched controls was increased in the COPD muscles661. Lactic acidosis is a
consequence of anaerobic metabolism in muscles, and progressively incremental exercise testing
can identify gradual a period when lactate accumulation increases sharply, termed �anaerobic
threshold’662. Lactate accumulation contributes strongly to muscle fatigue. This will occur sooner
650
Lawler JM, Song W, Demaree SR. Hindlimb unloading increases oxidative stress and disrupts
antioxidant capacity in skeletal muscle. Free Rad Biol Med 2003; 35:9-16
651
Vina J, Servera E, Asensi M, et al. Exercise causes blood glutathione oxidation in chronic obstructive
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Chandel NS, Trzyna WX, McClintock DS, Schumacker PT. Role of oxidants in NF-kappa B activation
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653
Yoshida Y, Maruyama M, Fujita T, et al. Reactive oxygen intermediates stimulate interleukin-6
production in human bronchial epithelial cells. Am J Physiol 1999; 276:L900-L908
654
Rabinovich RA, Figueras M, Ardite E, Carbo N, et al. Increased tumour necrosis factor-О± plasma levels
during moderate-intensity exercise in COPD patients. Eur Respir J 2003; 21:789-794
655
Ostrowski K, Scherling P, Pedersen BK. Physical activity and interleukin-6 in humans – effect of
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656
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Koechlin C, Maltais F, Saey D, et al. Hypoxaemia enhances peripheral muscle oxidative stress in
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Allaire J, Maltais F, LeBlanc P, Simard PM, et al. Lipofucsin accumulation in the vastus lateralis muscle
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Fluck. Hypoxaemia enhanced peripheral muscle oxidative stress in COPD. Thorax 2005; 60:797-798
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Barreiro E, de la Puente B, Minguella J, et al. Oxidative stress and respiratory muscle dysfunction in
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where oxygen supply is impaired, but usually occurs at around 45-65% of VO2max. It can be
reasoned that monitoring lactate might provide an index of muscle fatigue, and it is feasible to
measure lactate during walking exercise to help determine when rehabilitation may be indicated
or contraindicated, what exercise should be prescribed, and how patients are progressing with
rehabilitation663. It has also been shown that infusion of dichloroacetate (which delays onset of
anaerobic metabolism) can reduce blood lactate during maximal exercise in patients with COPD,
with consequent improvement in maximal exercise capacity664.
The roles of local and systemic inflammation665, oxidant / antioxidant imbalance666 and the
proposition of an active myopathy667 have been usefully summarised recently, along with the
nutritional and muscle consequences668. An interesting proposal has been examined in a crosssectional Belgian study, showing lower testosterone levels and higher follicle-stimulating and
luteinizing hormone levels in 50% of the 78 men with COPD than in 21 age-matched controls,
even in those not using corticosteroids and without hypoxaemia. These features correlated with
quadriceps muscle weakness and C-reactive protein, suggesting inflammation may be one
underlying mechanism of muscle weakness through gonadal suppression669. The plausibility of
this finding might be inferred from studies showing improved quadriceps force resulting from
testosterone supplementation, either with or without resistance exercise training670.
Physical Training
Barach pioneered the idea that exercise may be of some use for patients with respiratory
diseases671. Previously, rest and avoiding breathlessness were the recommended treatments for
most chronic respiratory conditions. Pierce reported one of the first studies on the benefits of
exercise retraining in COPD, finding that it enabled subjects to perform at the same level of
exercise capacity with lower heart-rate, respiratory rate, minute ventilation and CO2
production672. Since then there have been many observations, experimental findings and
randomised controlled trials confirming beneficial outcomes from exercise retraining.
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Tanaka Y, Hino M, Morikawa T, et al. Arterial blood lactate is a useful guide to when rehabilitation
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664
Calvert LD, Shelley R, Singh S, et al. Dichloroacetate enhances performance and reduces blood lactate
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Wouters EFM. Local and systemic inflammation in chronic obstructive pulmonary disease. Proc Am
Thorac Soc 2005; 2:26-33
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MacNee W. Pulmonary and systemic oxidant/antioxidant imbalance in chronic obstructive pulmonary
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668
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Van Vliet M, Spruit MA, Verleden G, et al. Hypogonadism, quadriceps weakness, and exercise
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670
Casaburi R, Bhasin S, Cosentino L, et al. Effects of testosterone and resistance training in men with
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671
Barach AL, Bickerman HA, Beck G. Advances in the treatment of non-tuberculous pulmonary disease.
Bull NY Acad Med 1952; 28:353-384
672
Pierce AK, Taylor HF, Archer RK, Miller WF. Responses to exercise training in patients with
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Mechanisms of exercise intolerance in COPD
The mechanisms underlying exercise performance impairment and improvement from exercise in
COPD are complex. Healthy people do not experience ventilatory limitation of exercise, while
those with COPD do673. People with COPD have reduced ventilatory capacity (e.g. reduced
forced expiratory volume in one second, FEV1)674, with reduced maximum ventilation at the
limits of their exercise capacity (VEmax)675 and often retain significant cardiac reserve676. The
low ventilatory capacity in turn leads to uneven distribution of ventilation and therefore increased
dead space, with resultant abnormal gas exchange and oxygen desaturation during exercise,
accompanied by reduced gas transfer677. The oxygen cost of breathing is high in people with
severe COPD678, and there may be weakness of the muscles of ventilation in some.
Dyspnoea refers to discomfort with breathing, so it is the perception rather than the sensation (e.g.
of rapid breathing) that delineates the symptom. The American Thoracic Society provided a
helpful consensus statement in 1999 on mechanisms and management of dyspnoea679, and a
conference devoted to the pathophysiology of dyspnoea has recently given an excellent series of
insights680. How people describe their sensations can be quite variable, and efforts have been
made over the years to clarify the descriptors of both stable and induced dyspnoea681,682, even
trying to delineate patterns of descriptors for specific pathophysiologic conditions.
In people with severe COPD, expiratory airflow limitation occurs during tidal breathing at
rest683,684, and the only way that ventilation can be sustained during exercise is to increase
ventilation rate685 and/or functional residual capacity (FRC). The latter results in restricted
673
Pardy RL, Hussain SNA, Macklem PT. The ventilatory pump in exercise. Clin Chest Med 1984; 5:35-
49
674
Dillard TA, Piantadosi S, Rajagopal KR. Determinants of maximum exercise capacity in patients with
chronic airflow obstruction. Chest 1989; 96:267-271
675
Spiro SG, Hahn HL, Edwards RHT, Pride NB. An analysis of the physiologic strain of submaximal
exercise in patients with chronic obstructive pulmonary disease. Thorax 1975; 30:415-425
676
Ortega F, Montemayor T, Sanchez A, Cabello F, Castillo J. Role of cardiopulmonary exercise testing
and the criteria used to determine disability in patients with severe chronic obstructive pulmonary disease.
Am J Respir Crit Care Med 1994; 150:747-751
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Jones NL, Jones G, Edwards HT. Exercise tolerance in chronic airways obstruction. Am Rev Respir Dis
1971; 103:477-491
678
Levison H, Cherniak RM. Ventilatory cost of exercise in chronic obstructive pulmonary disease. J Appl
Physiol 1968; 25:21-27
679
Meek PM, Schwartzstein RM, Adams L, et al for the American Thoracic Society. Dyspnea.
Mechanisms, assessment, and management: a consensus statement. Am J Respir Crit Care Med 1999;
159:321-340
680
O’Donnell DE, Banzett RB, Carrieri-Kohlman V, Casaburi R, et al. Pathophysiology of dyspnea in
chronic obstructive pulmonary disease. A roundtable. Proc Am Thorac Soc 2007; 4:145-168
681
Elliott MW, Adams L, Cockcroft A, et al. The language of breathlessness. Use of verbal descriptors by
patients with cardiopulmonary disease. Am Rev Respir Dis 1991; 144:826-832
682
Harver A, Mahler DA, Schwartzstein RM, Baird JC. Descriptors of breathlessness in healthy
individuals. Distinct and separable constructs. Chest 2000; 118:679-690
683
Stubbing DG, Pengelly LD, Morse JLC, Jones NL. Pulmonary mechanics during exercise in subjects
with chronic airflow limitation. J Appl Physiol 1980; 49:511-515
684
Baydur A, Milic-Emili J. Expiratory flow limitation during spontaneous breathing. Comparison of
patients with restrictive and obstructive respiratory disorders. Chest 1997; 112:1017-1023
685
Loveridge B, West P, Kryger MH, Anthonisen NR. Alteration in breathing pattern with progression of
chronic obstructive pulmonary disease. Am Rev Respir Dis 1986; 134:930-934
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inspiratory capacity (IC)686, and end-inspiratory volume during tidal breathing in exercise may
approach total lung capacity (TLC)687. The IC/TLC ratio has recently come to be known as the
“inspiratory fraction”688, in an attempt to develop a functional index that predicts risk of death
like a functional cardiac index in ischaemic heart disease. The value of the inspiratory fraction in
predicting maximum exercise tolerance (disability) has also been examined and confirmed
recently689. The former prevents satisfactory lung emptying, and contributes to dynamic
hyperinflation, as described by O’Donnell690,691, Ferguson692,693, and Price694. Dynamic
hyperinflation (DH) causes marked increase in work of breathing, with onset of dyspnoea and
limitation of inspiratory muscles endurance695, and these act together to reduce exercise
capacity696.
Measurement of operational lung volumes has helped to understand and explain exercise
limitation imposed by DH and the effects of interventions. A new tool for assessment of breathby-breath variations of the volume of the rib cage and abdominal compartments is optoelectronic
plethysmography (OEP)697,698. The effects of drugs and training on chest wall dimensions during
exercise have been well described, and correlations between end-expiratory abdominal volume
and improved exercise performance have been demonstrated699. The changes in chest wall
volumes (specifically end-expiratory abdominal volume) with DH of exercise are modified by the
severity of airflow limitation (i.e. COPD severity), such that greater degrees of chest wall DH
occur in more severe COPD and result in less displacement of abdominal volume with greater
increase in end-expiratory ribcage volume700. This difference helps to account for the reduced
minute ventilation people with severe COPD can generate during exercise. People with Stages I
and II COPD closely resemble normal healthy individuals in their chest wall mechanics during
686
Koulouris NG, Dimopoulou I, Valta P, Finkelstein R, et al. Detection of expiratory flow limitation
during exercise in COPD patients. J Appl Physiol 1997; 82:723-731
687
O'Donnell DE, Webb KA. Exertional breathlessness in patients with chronic airflow limitation: the role
of lung hyperinflation. Am Rev Respir Dis 1993; 18:1351-1357
688
Casanova C, Cote C, Torres JP, et al. Inspiratory-to-total lung capacity ratio predicts mortality in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2005; 171:591-597
689
Albuquerque ALP, Nery LE, Villaca DS, Machado TYS, et al. Inspiratory fraction and exercise
impairment in COPD patients GOLD stages II-III. Eur Respir J 2006; 28:939-944
690
O'Donnell DE, Webb KA. Exertional breathlessness in patients with chronic airflow limitation: the role
of lung hyperinflation. Am Rev Respir Dis 1993; 18:1351-1357
691
O’Donnell DE. Hyperinflation, dyspnea, and exercise intolerance in chronic obstructive pulmonary
disease. Proc Am Thorac Soc 2006; 3:180-184
692
Ferguson GT. The ins and outs of breathing: an overview of lung mechanics. Eur Respir Rev 2004;
13:30-34
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Ferguson GT. Why does the lung hyperinflate? Proc Am Thorac Soc 2006; 3:176-179
694
Price D, Freeman D, Kaplan A, Ostrem A, et al. Progressive breathlessness in COPD – The role of
hyperinflation and its pharmacological management. Primary Care Respir J 2005; 14:285-293
695
Tzelepsis G, McCool FD, Leith DE, Hoppin FG. Increased lung volume limits endurance of inspiratory
muscles. J Appl Physiol 1988; 64:1796-1802
696
Murariu C, Ghezzo H, Milic-Emili J, Gautier H. Exercise limitation in obstructive lung disease. Chest
1998; 114:965-968
697
Aliveri A, Stevenson N, Dellaca RL, et al. Regional chest wall volumes during exercise in chronic
obstructive pulmonary disease. Thorax 2004; 59:210-216
698
Vogiatzis I, Georgiadou O, Golemati S, et al. Patterns of dynamic hyperinflation during exercise and
recovery in patients with severe chronic obstructive pulmonary disease. Thorax 2005; 60:723-729
699
Georgiadou O, Vogiatzis I, Stratokos G, et al. Effects of pulmonary rehabilitation on operational chest
wall volumes during exercise in COPD patients. Eur Respir J 2007; 29:284-291
700
Vogiatziz I, Stratokos G, Athanasopoulos D, et al. Chest wall volume regulation during exercise in
COPD patients with GOLD Stages II to IV. Eur Respir J 2008; 32:42-52
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exercise, even if resting hyperinflation is present, meaning expiratory (especially abdominal)
muscles are recruited to reduce end-expiratory abdominal volume and thereby minimize the chest
wall hyperinflation. In more severe COPD (Stages III and IV) this phenomenon cannot be
sustained, and the chest wall and tidal volumes become progressively restricted, and these
patients stop exercise because of dyspnoea.
DH may be a contributor to hypercapnia in the stable resting state in patients with severe COPD
(in addition to weakness of the ventilatory muscles)701. Further, the skeletal muscles of people
with severe COPD are often unable to sustain repetitive contraction, and they fatigue
prematurely, so that patients are unable to perform activities of daily living (ADLs) with
comfort702,703. Neuromuscular fatigue appears to be a direct cause in many patients704. The
discovery of the importance (and mechanisms) of dynamic hyperinflation has led to clarification
of the way various interventions improve breathlessness and exercise performance705.
Fatigue, muscle weakness and HRQoL are interrelated. First, the ability to perform ADLs - which
is determined by lung physiology, muscle and exercise function - is the chief component of
functional status. Second, high levels of dyspnoea or fatigue with ADLs, muscle weakness, or
avoidance of ADLs all influence perceived HRQOL. Third, HRQoL combines the physical and
mental impacts of functional status706,707,708,709,710. In a study of 132 Japanese patients with FEV1
41.3% predicted (SD 19.0%), generic and lung-specific HRQoL were measured along with postbronchodilator lung function. HRQoL was partly explained by airflow limitation (odds ratio,
OR=0.59-0.69), diffusing capacity (OR=0.75-0.82), smoking history (OR=1.20-1.23) and age
(OR=2.13), though their overall contribution was limited711.
Many of the premises on which exercise training in COPD are based derive from training in
normal individuals. Strategies may need to be altered depending on the severity of COPD and the
presence and severity of DH (see above), although this hypothesis has not yet been evaluated in
the current literature. Changes in understanding limitations of exercise in COPD have rather
inhibited standardisation of exercise training regimens in COPD until recent years, and this makes
701
Montes de Oca M, Celli BR. Respiratory muscle recruitment and exercise performance in eucapnic and
hypercapnic severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000; 161:880-885
702
Decramer M, Gosseling R, Troosters T, Verschueren M, Evers G. Muscle weakness is related to
utilization of health care resources in COPD patients. Eur Respir J 1997; 1-:417-423
703
Yohannes AM, Roomi J, Waters K, Connolly MJ. Quality of life in elderly patients with COPD:
measurement and predictive factors. Respir Med 1998; 92:1231-1236
704
Maltais F, Jobin J, Sullivan MJ, et al. Metabolic and hemodynamic responses of lower limb during
exercise in patients with COPD. J Appl Physiol 1998; 83:1573-1580
705
Casaburi R, Porszasz J. Reduction of hyperinflation by pharmacologic and other interventions. Proc Am
Thorac Soc 2006; 3:185-189
706
Reardon JZ, Lareau SC, ZuWallack R. Functional status and quality of life in chronic obstructive
pulmonary disease. Am J Med 2006; 119 (Suppl 1):32-37
707
Stavem K, Boe J, Erikssen J. Health status, dyspnea, lung function and exercise capacity in patients with
chronic obstructive pulmonary disease. Internat J Tuberc Lung Dis 1999; 3:920-926
708
Fuchs-Climent D, La Gallais D, Varray A, et al. Factor analysis of quality of life, dyspnea, and
physiologic variables in patients with chronic obstructive pulmonary disease before and after rehabilitation.
Am J Phys Med Rehabil 2001; 80:113-120
709
Hajiro T, Nishimure K, Tsukino M, et al. A comparison of the level of dyspnoea vs disease severity in
indicating the health-related quality of life of patients with COPD. Chest 1999; 116:1632-1637
710
Monso E, Fiz JM, Izquierdo J, Alonso J, et al. Quality of life in severe chronic obstructive pulmonary
disease: correlation with lung and muscle function. Respir Med 1998; 92:221-227
711
Tsukino M, Nishimura K, Ikeda A, Koyama H, et al. Physiologic factors that determine the healthrelated quality of life in patients with COPD. Chest 1996; 110:896-903
92
firm conclusions about the reasons for improved exercise performance with exercise training
difficult. The consensus of research is that improvements from training do not require major
change in lung function. Other mechanisms include improved aerobic capacity, muscle strength
and ventilatory muscle function, more effective integration of chest wall and abdominal
mechanics to limit DH, increased motivation, desensitisation to the sensation of dyspnoea, and
improved technique of test performance. These mechanisms and the evidence base related to
exercise training in COPD have been subjected to careful literature review, with regular updates.
Physiotherapists have led the way in developing multi-modality exercise training for patients
requiring post-operative rehabilitation, for those recovering from acute events like “Strokes” or
myocardial infarctions, and for those with chronic disabling conditions like COPD. They have
built upon information developed in healthy individuals and athletes by exercise physiologists.
Often the programs developed by physiotherapists have concentrated on exercise training as the
lead or sole component in pulmonary �rehabilitation’ programs. Indeed, most of the evidence for
improved exercise capacity is based on physical training. Exercise is therefore a vital component
of pulmonary rehabilitation712, and usually includes activities, task optimisation to reduce
unnecessary energy expenditure, breathing control during exertion, and pursed lip breathing, in
addition to aerobic training of upper and lower limbs as well as trunk muscles.
Overall activity levels have been correlated with daily fatigue, dyspnoea and health status in
patients with COPD713. Benefits are not related to initial lung function714, so PR should be
applicable to any Stage of Severity of COPD. It may also be applicable to other respiratory
conditions, such as asthma715, bronchiectasis716 and interstitial disorders717. Recent surveying of
422 patients completing PR revealed 309 patients with COPD and 113 with non-COPD
diagnoses, and no systematic or significant differences were seen between these two groups in 6minute walk or quality of life improvements718.
Physiologic training effects can be demonstrated in people with COPD following sustained and
repeated exercise at or above anaerobic threshold719. Muscle metabolism, such as oxygen
extraction, can be improved even by submaximal exercise in people with COPD720. More specific
aspects of training are provided below. These training effects might be enhanced by reducing
ventilatory loading through providing positive pressure assistance721, with oxygen therapy, or
712
Rochester CL. Exercise training in COPD. J Rehabil Res Develop 2003; 40:59-88
Roberts S, Langley C, Tregonning M, Duffy H, et al. Activity levels in COPD are related to fatigue and
general health status but not to lung function. Thorax 1999; 54:A55
714
Niederman MS, Clemente PH, Fein AM, Feinsilver SH, et al. Benefits of a multidisciplinary pulmonary
rehabilitation program. Improvements are independent of lung function. Chest 1991; 99:798-804
715
Cambach W, Wagenaar RC, Koelman TW, et al. The long-term effects of pulmonary rehabilitation in
patients with asthma and chronic obstructive pulmonary disease: a research synthesis. Arch Phys Med
Rehabil 1999; 80:103-111
716
Bradley J, Moran F, Greenstone M. Physical training for bronchiectasis. Cochrane Database Syst Rev
2006; Issue 4
717
Naji NA, Connor MC, Donnelly SC, McDonnell TJ. Effectiveness of pulmonary rehabilitation in
restrictive lung disease. J Cardiopulm Rehabil 2006; 26:237-243
718
Ferreira G, Feuerman M, Spiegler P. Results of an 8-week, outpatient pulmonary rehabilitation program
on patients with and without chronic obstructive pulmonary disease. J Cardiopulm Rehabil 2006; 26:54-60
719
Casaburi R, Patessio A, Ioli F, Zanaboni S, et al. Reductions in exercise lactic acidosis and ventilation as
a result of exercise training in patients with obstructive lung disease. Am Rev Respir Dis 1991; 143:9-18
720
Sala E, Roca J, Marrades RM, Alonso J, et al. Effects of endurance training on skeletal muscle
bioenergetics in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999; 159:1726-1734
721
Polkey MI, Hawkins P, Kyroussis D, Ellum SG, et al. Inspiratory pressure support prolongs exercise
induced lactataemia in severe COPD. Thorax 2000; 55:547-549
713
93
with medications such as ipratropium722 and salmeterol723. In a recent randomised controlled trial,
a three-month program improved HRQoL in both males and females, and while continuing
supervised training for up to 18 months had no added benefit in females, it did in males724. The
effects of oxygen therapy and of ventilatory assistance need brief additional discussion.
Exercise Prescription
Formal cardiopulmonary exercise testing is expensive, technically demanding, and often daunting
for older people and those with COPD. Other options for estimating VO2max are therefore often
used to estimate a person’s exercise capacity for training. In people with COPD or heart failure,
for example, a 6-minute walk test may be attractive because of the correlation between 6MWD
and VO2max725. However the confidence limits of these inter-relationships are wide726 and the
exercise demands are quite different727. Attempts have been made to strengthen prediction of
VO2max using not only 6MWD but also patient weight, although subsequently this was shown to
be unreliable728. It is therefore recommended that, if VO2max is used in training prescriptions, it
be measured directly. Activity-specific training plus aerobic training over 10 weeks has shown
greater benefit than exercise training alone or with an education lecture program in a randomized
study of 43 patients with COPD729. Such an approach requires higher degrees of supervision, but
is likely to enhance self-efficacy for exercise, and therefore the likelihood that exercise will be
maintained after completion of the formal program.
Supervision of training
Supervision of exercise training is recommended at least initially so that the therapist can
appreciate the limits to exercise, evaluate breathing pattern and individual mechanisms of fatigue,
and help to build the patient’s confidence so improved cardiovascular fitness can be achieved.
While some benefit can be gained from low-intensity training, higher intensity training (at a heart
rate at or above anaerobic threshold) is more effective730,731. Flexibility and muscle strength
should also be addressed. The mode of training (endurance versus strength) determines the
outcomes in athletes732, and there is some evidence that this is also true in COPD733. Training
722
O’Donnell DE, Lam M, Webb KA. Spirometric correlates of improvement in exercise performance after
anticholinergic therapy in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999;
160:542-549
723
Patakas D, Andreadis D, Mavrofridis E, Argyropoulou P. Comparison of the effects of salmeterol and
ipratropium bromide on exercise performance and breathlessness in patients with stable chronic obstructive
pulmonary disease. Respir Med 1998; 92:1116-1121
724
Foy CG, Rejeski J, Berry MJ, et al. Gender moderates the effects of exercise therapy on health0related
quality of life among COPD patients. Chest 2001; 119:70-76
725
Cahalin L, Pappagianopoulos P, Prevost S, et al. The relationship of the 6-min walk test to maximum
oxygen consumption in transplant candidates with end-stage lung disease. Chest 1995; 108:452-459
726
Carlson DJ. VO2max: the gold standard? Chest 1995; 108:602-603
727
Cavagna GA, Saibene FP, Margaria R. External work in walking. J Appl Physiol 1963; 18:1-9
728
Chuang ML, Lin IF, Vintch JRE. Comparison of estimated and measured maximal oxygen uptake
during exercise testing in patients with chronic obstructive pulmonary disease. Intern Med J 2004; 34:469474
729
Norweg AM, Whiteson J, Malgady R, et al. The effectiveness of different combinations of pulmonary
rehabilitation program components. A randomised controlled trial. Chest 2005; 128:663-672
730
Casaburi R, Patessio A, Ioli F, Zanaboni S, Donner CF, Wasserman K. Reductions in exercise lactic
acidosis and ventilation as a result of exercise training in patients with obstructive lung disease. Am Rev
Respir Dis 1991; 143:9-18
731
Puente-Maestu L, Sanz ML, Sanz P, et al. Effects of two types of training on pulmonary and cardiac
responses to moderate exercise in patients with COPD. Eur Respir J 2000; 15:1026-1032
732
Maughan R, Gleeson M, Greenhaff PL. Biochemistry of exercise and training. Oxford: Oxford
University Press. 1997
94
benefits are usually progressively lost after initial intensive training so maintenance of activities
is essential for continuing the benefits. In a West Australian study, 12 months of physiotherapistsupervised weekly community-based maintenance exercise classes were provided after formal
exercise-based PR. Over 4 years, of the 497 patients referred to PR 172 completed the full course,
of whom a minority completed the maintenance classes for at least 12 months (n=46).
Improvements made in CRQ quality of life and 6-minute walk distance during PR were
maintained (at the clinically significant level) in the regular maintenance patients with moderatesevere COPD, and 67% of these patients were performing their own home exercises 3 to 5 days a
week as well734.
It is feasible for suitably-trained exercise scientists to provide the level of supervision for
maintenance classes, and to be involved in some initial physical training, though this would
preferably be under medical supervision or in conjunction with physiotherapists.
Substantial evidence exists for the benefits of general (multi-modality) exercise training, with
randomised controlled trials demonstrating improvements in exercise tolerance, well-being,
symptoms of dyspnoea, and self-efficacy735,736,737,738. The effects of exercise training on exercise
performance are greater than education alone739. Physical training usually includes both strength
and endurance training. While optimal intensity, frequency, duration and length of training are yet
to be determined, some guidelines for exercise prescription can be suggested, as below.
733
Ortega F, Toral J, Cejudo P, et al. Comparison of effects of strength and endurance training in patients
with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2002; 166:669-674
734
Cockram J, Cecins N, Jenkins S. Maintaining exercise capacity and quality of life following pulmonary
rehabilitation. Respirology 2006; 11:98-104
735
Cockcroft AE, Saunders MJ, Berry G. Randomised controlled trial of rehabilitation in chronic
respiratory disability. Thorax 1981; 36:200-203
736
McGavin CR, Gupta SP, Lloyd EL, McHardy GJR. Physical rehabilitation for the chronic bronchitic:
results of a controlled trial of exercises in the home. Thorax 1977; 32:307-311
737
Casaburi R. Exercise training in chronic obstructive lung disease. In: Casaburi R, Petty TL (Eds)
Principles and Practice of Pulmonary Rehabilitation. Philadelphia PA. WB Saunders. 1993
738
Hernandez MTE, Rubio TM, Ruiz FO, Riera HS, et al. Results of a home-based training program for
patients with COPD. Chest 2000; 118:106-114
739
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995;
122:823-832
95
FIGURE 4.3
PHYSIOTHERAPISTS NEED TO SUPERVISE TRAINING DIRECTLY IN INITIAL PHASES
OF PULMONARY REHABILITATION GYM SESSIONS
Endurance Training
Endurance muscle training can increase the oxidative capacity of skeletal muscles740 (impaired in
patients with COPD, as discussed above), and reduce fatiguability of the muscles741. In a
systematic review, which included 15 satisfactory randomized controlled trials of exercise
intensity or modality of endurance training, there were inconsistent findings across studies742,
some showing greater benefits from endurance training, and others with better outcomes from
strength training. In five trials that compared endurance training with combined strength and
endurance training, little gain was found in exercise capacity or health status. People with FEV1
below 40% predicted are unlikely to undertake endurance training, though they are usually able to
do interval training743.
Interval training has also been evaluated, with alternating high and low intensity periods during
individual training sessions, and no real difference has been found compared to constant work
rate exercise in terms of endurance outcomes744,745. This suggests that these modalities could be
740
Maltais F, Leblanc P, Simard C, et al. Skeletal muscle adaptation to endurance training in patients with
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1996; 154:442-447
741
Mador MJ, Kufel TJ, Pineda LA, et al. Effect of pulmonary rehabilitation on quadriceps fatiguability
during exercise. Am J Respir Crit Care Med 2001; 163:930-935
742
Puhan MA, Schunemann HJ, Frey M, et al. How should patients with COPD exercise during respiratory
rehabilitation? Comparison of exercise modalities and intensities to treat skeletal muscle dysfunction.
Thorax 2005; 60:367-375
743
Troosters T, Gosselink R, Decramer M. Exercise training: how to distinguish responders from nonresponders. J Cardiopulm Rehabil 2001; 21:10-17
744
Coppoloose R, Schols AM, Baarends EM, et al. Interval versus continuous training in patients with
severe COPD: a randomized clinical trial. Eur Respir J 1994; 14:258-263
96
used interchangeably, depending on the individual patients’ preferences and capabilities, or even
according to the limitations imposed by the training venue, equipment or staff.
As indicated several times, maintenance of exercise following completion of a PR program is
vital, as the benefits of exercise training gradually disappear if this does not happen. A recent
intervention trial involving 123 patients who completed PR followed by supervised regular
walking over 12 months and observation over the next 12 months, showed that those who did
persist with regular walking (active essentially every day through 24 months) had slower declines
in dyspnoea with ADLs, health status and walking self-efficacy746.
Intensity and Progression
Effective training modalities use one or other of the following initial targets for exercise intensity:
• 60% maximum power output or peak VO2 from a cycle ergometry test747,748.
• 60% of the maximal walking speed achieved on an incremental shuttle walk test.
Dyspnoea score749 appears a more effective monitoring method than heart rate750 in COPD,
although mechanical efficiency appears to improve more than VO2751, particularly for whole
body exercise752 - whole body exercise conducted as interval cycling to high rates, treadmill
walking as continuous exercise, and short blocks of stair climbing, all of which have different
metabolic demands and responses. Progression of each style needs individual attention.
Patients with moderate to severe COPD demonstrate dynamic hyperinflation (DH), as described
above. This increases with the increased ventilation demanded in sustained exercise, and this DH
can compromise cardiac performance through increasing intra-thoracic pressure. The combined
effects limit exercise endurance, and it has been shown that interval exercise rather than constantload exercise can moderate these effects and enhance training753. A greater total duration of
exercise can be achieved using this modality, a finding confirmed in a small (n=10) comparison
of intermittent exercise to low VO2 with a sustained exercise regimen754, where greater total
energy expenditure was achieved with less DH with the intermittent regimen.
745
Puhan MA, Busching G, Schunemann HJ, et al. Interval versus continuous high-intensity exercise in
chronic obstructive pulmonary disease: a randomized trial. Annals Intern Med 2006; 145:816-825
746
Heppner PS, Morgan C, Kaplan RM, Ries AL. Regular walking and long-term maintenance of outcomes
after pulmonary rehabilitation. J Cardiopulm Rehabil 2006; 26:44-53
747
Maltais F, LeBlanc P, Jobin J, et al. Intensity of training and physiological adaptation in patients with
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1997; 155:555-561
748
Troosters T, Casaburi R, Gosselink R, Decramer M. Pulmonary rehabilitation in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 2005; 172:19-38
749
Mejia R, Ward J, Lentine T, Mahler DA. Target dyspnea ratings predict expected oxygen consumption
as well as target heart rates. Am J Respir Crit Care Med 1999; 159:1485-1489
750
Zacarias EC, Neder JA, Cendom SP, et al. Heart rate at the estimated lactate threshold in patients with
chronic obstructive pulmonary disease: effects on the target intensity for dynamic exercise testing. J
Cardiopulm Rehabil 2000; 20:369-376
751
Milani RV, Lavie CJ. Disparate effects of out-patient cardiac and pulmonary rehabilitation programs on
work efficiency and peak aerobic capacity in patients with coronary disease or severe obstructive
pulmonary disease. J Cardiopulm Rehabil 1998; 18:17-22
752
Probst VS, Troosters T, Pitta F, et al. Cardiopulmonary stress during exercise training in patients with
COPD. Eur Respir J 2006; 27:1110-1118
753
Vogiatzis I, Nanas S, Kastanakis E, Georgiadou O, et al. Dynamic hyperinflation and tolerance to
interval exercise in patients with advanced COPD. Eur Respir J 2004; 24:385-390
754
Sabapathy S, Kingsley RA, Schneider DA, et al. Continuous and intermittent exercise responses in
individuals with chronic obstructive pulmonary disease. Thorax 2004; 59:1026-1031
97
Frequency
Based on training observations made in healthy people, training effects have been evaluated in
people with COPD, and effects can be demonstrated with 3 to 5 sessions per week (but not with
two sessions a week) 755. It has been recommended to have at least two of these sessions
supervised756.
Duration
Again based on studies in healthy individuals, each session should ensure the recommended
intensity levels are reached for 20 to 30 minutes757.
Mode
There should be a mix of leg exercise (such as walking and/or stationary cycling) and arm
training, including unsupported arm exercise to improve overall exercise capacity758.
Hydrotherapy may be favoured by some patients, and is feasible759, though there is no good
evidence for benefit (or harm).
Course Duration
Courses should run for at least four weeks, and preferably up to 12 weeks. There is a gradient of
benefit with increasing duration760,761,762.
Training benefits decline if training stops. Participation in regular walking following completion
of PR is associated with better maintenance of HRQoL and walking self-efficacy, together with
less dyspnoea763. Behavioural techniques can improve adherence to continuing exercise
regimens764. Musical distraction is a well-known device in healthy populations undertaking
exercise training. Distractive auditory stimuli can reduce perceived exertion in people with COPD
during training and to increase their total exercise time765, and in other areas to reduce anxiety
755
Ringbaek TJ, Bioendum E, Hemmingsen L, et al. Rehabilitation of patients with chronic obstructive
pulmonary disease. Exercise twice a week is not sufficient! Respir Med 2000; 94:150-154
756
Sala E, Roca J, Marrades RM, et al. Effects of endurance training on skeletal muscle bioenergetics in
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999; 159:1726-1734
757
Casaburi R. Exercise training in chronic obstructive lung disease. In: Casaburi R, Petty TL (Eds)
Principles and Practice of Pulmonary Rehabilitation. Philadelphia PA. WB Saunders; 1993
758
Lake FR, Henderson K, Briffa T, et al. Upper-limb and lower-limb exercise training in patients with
chronic airflow obstruction. Chest 1990; 97:1077-1082
759
Perk J, Perk L, Boden C. Cardiorespiratory adaption of COPD patients to physical training on land and
in water. Eur Respir J 1996; 9:248-252
760
Casaburi R. Exercise training in chronic obstructive lung disease. In: Casaburi R, Petty TL (Eds)
Principles and Practice of Pulmonary Rehabilitation. Philadelphia PA. WB Saunders; 1993
761
Maltais F, LeBlanc P, Jobin J, et al. Intensity of training and physiological adaptation in patients with
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1997; 155:555-561
762
Green RH, Singh SJ, Williams J, Morgan MDL. A Randomized trial of four weeks versus seven weeks
of pulmonary rehabilitation in chronic obstructive pulmonary disease. Thorax 2001; 56:143-145
763
Heppner PS, Morgan C, Kaplan RM, Ries AL. Regular walking and long-term maintenance of outcomes
after pulmonary rehabilitation. J Cardiopulm Rehabil 2006; 26:44-53
764
Kaplan RM, Ries AL, Prewitt LM, et al. Self-efficacy expectations predict survival for patients with
chronic obstructive pulmonary disease. Health Psychol 1994; 13:366-368
765
Thornby MA, Haas F, Axen K. Effect of distractive auditory stimuli in exercise tolerance in patients
with COPD. Chest 1995; 107:1213-1217
98
during a variety of interventions766,767,768. This approach was trialled in 24 patients with moderate
to severe COPD following PR, in a randomised controlled trial, with either encouragement to
continue unsupervised walking or encouragement plus portable audiocassette tape with selfselected music to be used during walking769. Cumulative distances logged on pedometer were
24% higher in the auditory distraction group, and there was significantly lower perceived exertion
during ADL. The distraction group increased average 6-minute walk distances by another 445
feet compared to the encouragement-only group having a fall in 6-minute walk distance
averaging 169 feet. This may be a cost-effective way for helping patients continue exercise
following PR and thereby maintain or build on their gains.
The question of consolidation PR – follow-up enrolment in another 8-week program a year after
an initial course, as discussed above - has been addressed in Italy770. Thirty-six patients were
studied before, a year after PR and another year later after half had undergone a second course.
Both groups had a range of initial improvements, and added long-term effects of a second course
were maintenance of lower rates of hospitalisation with exacerbations in the second year.
Strength Training
Skeletal muscle mass is low and weakness is present in many patients with moderate-severe
COPD, and can affect both upper and lower limbs771. Strength training in such patients can
improve muscle strength772, peak work capacity773 and endurance time774. A combination of
strength and endurance training results in greater increases in both strength and endurance than
either form of training alone775,776. A randomised trial of endurance training over 8 weeks
compared to the same regimen of endurance training plus sets of five muscle group incrementing
resistance training exercises over the 8 weeks showed strength increased in the strength-trained
group and declined in the endurance-only group. More importantly, perhaps, functional fitness
improvements were greater when strength training was added to endurance training777. More
recently, 32 consecutive elderly patients with moderately-severe COPD were clustered into
766
Binnings EB. The effect of an auditory distraction on anxiety in ambulatory surgical patients
experiencing regional anaesthesia. AANA J 1987; 55:333-335
767
Chlan L. Effectiveness of a music therapy intervention on relaxation and anxiety for patients receiving
ventilatory assistance. Heart Lung 1998; 27:169-176
768
Zimmerman L, Pierson M, Marker J. Effects of music on patient anxiety in coronary care units. Heart
Lung 1988; 17:560-566
769
Bauldof GS, Hoffman LA, Zullo TG, Sciurba FC. Exercise maintenance following pulmonary
rehabilitation. Effect of distractive stimuli. Chest 2002; 122:948-954
770
Foglio K, Bianchi L, Ambrosino N. Is it really useful to repeat outpatient pulmonary rehabilitation
programs in patients with chronic airways obstruction? A 2-year controlled study. Chest 2001; 119:16961704
771
Simpson K, Killian K, McCartney N, et al. Randomised controlled trial of weightlifting exercise in
patients with chronic airflow limitation. Thorax 1992; 47:70-75
772
Simpson K, Killian K, McCartney N, et al. Randomised controlled trial of weightlifting exercise in
patients with chronic airflow limitation. Thorax 1992; 47:70-75
773
Spruit MA, Gosselink R, Troosters T, et al. Resistance versus endurance training in patients with COPD
and peripheral muscle weakness. Eur Respir J 2002; 19:1072-1078
774
Lake FR, Henderson K, Briffa T, et al. Upper-limb and lower-limb exercise training in patients with
chronic airflow obstruction. Chest 1990; 97:1077-1082
775
Ortega F, Toral J, Cejudo P, et al. Comparison of effects of strength and endurance training in patients
with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2002; 166:669-674
776
Bernard S, Wjittom L, LeBlanc P, et al. Aerobic and strength training in patients with chronic
obstructive pulmonary disease. Am J Respir Crit Care Med 1999; 159:896-899
777
Phillips WT, Benton MJ, Wagner CL, Riley C. The effect of single set resistance training on strength
and functional fitness in pulmonary rehabilitation patients. J Cardiopulm Rehabil 2006; 26:330-337
99
randomly-assigned groups that undertook endurance training alone or endurance training plus
strength training over 8 weeks, and again significant improvements were seen in strength of the
skeletal muscles in those doing combined exercises. However no differences were seen between
the groups in exercise performance or quality of life778.
A systematic review included nine trials involving a total of 236 patients with COPD. Substantial
gain in strength is possible in such patients779. However in only one trial could improved exercise
capacity (equivalent to endurance training) be found780, and there was no substantive evidence of
beneficial effects of strength training alone on health status or ADL functionality. On the other
hand, a more recent systematic review of 15 trials suggested some studies had found greater
improvements in quality of life from strength training than from endurance training781.
FIGURE 4.4
STRENGTH TRAINING OF SKELETAL MUSCLES MAY BE A USEFUL COMPONENT OF
PULMONARY EXERCISE TRAINING
778
Mador MJ, Bozkanat E, Aggarwal A, et al. Endurance and strength training in patients with COPD.
Chest 2004; 125:2036-2045
779
O’Shea SD, Taylor NF, Paratz J. Peripheral muscle strength training in COPD: a systematic review.
Chest 2004; 126:903-914
780
Spruit MA, Gosselink R, Troosters T, et al. Resistance versus endurance training in patients with COPD
and peripheral muscle weakness. Eur Respir J 2002; 19:1072-1078
781
Puhan MA, Schunemann HJ, Frey M, et al. How should patients with COPD exercise during respiratory
rehabilitation? Comparison of exercise modalities and intensities to treat skeletal muscle dysfunction.
Thorax 2005; 60:367-375
100
Specific muscle group training
Training of specific muscle groups (eg upper extremities782,783,784 compared to lower
extremities785, and inspiratory muscles786) provides benefits that are not as great as when all are
included787, and not all studies have shown consistent results. As indicated above, both strength
and endurance can be targeted788,789,790, but individual requirements need to be taken into account.
Upper Limb Training
Upper extremity training specifically improves arm function791,792,793,794,795,796. Unsupported arm
training is more effective than supported arm training797, and has proven metabolic training
effects798. Arm training alone was less effective than leg training or combined training at
improving overall exercise function799, but had an incremental benefit over leg training alone800.
782
Ries AL, Ellis B, Hawkins RW. Upper extremity exercise training in chronic obstructive pulmonary
disease. Chest 1988; 93:688-692
783
Couser JI, Martinez FJ, Celli BR. Pulmonary rehabilitation that includes arm exercise reduces metabolic
and ventilatory requirements for simple arm elevation. Chest 1993; 103:37-41
784
Martinez FJ, Vogel PD, Dupont DN, Stanopoulos I, et al. Supported arm exercise vs unsupported arm
exercise in the rehabilitation of patients with severe chronic airflow obstruction. Chest 1993; 103:13971402
785
Lake FR, Henderson K, Briffa T, et al. Upper-limb and lower-limb exercise training in patients with
chronic airflow obstruction. Chest 1990; 97:1077-1082
786
Smith K, Hook D, Guyatt GH, et al. Respiratory muscle training in chronic airflow limitation: metaanalysis. Am Rev Respir Dis 1992; 145:533-539
787
Belman MJ, Mohensifar Z. Reductions in exercise lactic acidosis and ventilation as a result of exercise
training in patients with obstructive lung disease. Am Rev Respir Dis 1991; 144:1220-1221
788
Punzal PA, Ries AL, Kaplan RM, Prewitt LM. Maximum intensity exercise training in patients with
chronic obstructive pulmonary disease. Chest 1991; 100:618-623
789
O’Hara WJ, Lasachuk KE, Matheson P, et al. Weight training and backpacking in COPD. Respir Care
1984; 29:1202-1210
790
Simpson K, Killian K, McCartney N, et al. Randomized controlled trial of weightlifting exercise in
patients with chronic airflow limitation. Thorax 1992; 47:70-75
791
Belman MJ, Kendregan BA. Exercise training fails to increase skeletal enzymes in patients with chronic
obstructive pulmonary disease. Am Rev Respir Dis 1981; 123:256-261
792
O’Hara WJ, Lasachuk KE, Matheson P, et al. Weight training and backpacking in COPD. Respir Care
1984; 29:1202-1210
793
Ries AL, Ellis B, Hawkins RW. Upper extremity exercise training in chronic obstructive pulmonary
disease. Chest 1988; 93:688-692
794
Lake FR, Henderson K, Briffa T, et al. Upper-limb and lower-limb exercise training in patients with
chronic airflow obstruction. Chest 1990; 97:1077-1082
795
Martinez FJ, Vogel PD, Dupont DN, Stanopoulos I, et al. Supported arm exercise vs unsupported arm
exercise in the rehabilitation of patients with severe chronic airflow obstruction. Chest 1993; 103:13971402
796
Couser JI, Martinez FJ, Celli BR. Pulmonary rehabilitation that includes arm exercise reduces metabolic
and ventilatory requirements for simple arm elevation. Chest 1993; 103:37-41
797
Martinez FJ, Vogel PD, Dupont DN, Stanopoulos I, et al. Supported arm exercise vs unsupported arm
exercise in the rehabilitation of patients with severe chronic airflow obstruction. Chest 1993; 103:13971402
798
Couser JI, Martinez FJ, Celli BR. Pulmonary rehabilitation that includes arm exercise reduces metabolic
and ventilatory requirements for simple arm elevation. Chest 1993; 103:37-41
799
Ries AL, Ellis B, Hawkins RW. Upper extremity exercise training in chronic obstructive pulmonary
disease. Chest 1988; 93:688-692
800
Lake FR, Henderson K, Briffa T, et al. Upper-limb and lower-limb exercise training in patients with
chronic airflow obstruction. Chest 1990; 97:1077-1082
101
Training of general or specific upper limb/pectoral girdle muscles may improve ventilatory
muscle function801, perhaps to the same extent as specific ventilatory muscle training802.
Ventilatory muscle training
The inefficiencies of the ventilatory muscle pump resulting from altered lung elastic recoil
associated with DH, and skeletal muscle weakness already described have encouraged the
concept of training ventilatory muscles. However, inspiratory muscles in COPD patients are
actually well-conditioned in comparison to control subjects, probably as an adaptive response to
constant loading of the muscles803, countering the general logic used in supporting inspiratory
muscle training (IMT). Despite this, there is evidence of benefit. In 1976 improved ventilatory
muscle strength after five weeks of ventilatory muscle strength training was described in normal
subjects, and improved ventilatory endurance after endurance training compared to control
individuals804. Benefits declined after 15 weeks of de-training805. An uncontrolled study of 10
patients with COPD before and after endurance IMT for six weeks found significant
improvement in maximal sustained ventilatory capacity, VO2 during maximal sustained
ventilatory capacity testing, and better maximal exercise capacity and 12-MWD806.
Most randomised studies to 1992 used inadequate training stimulus807, and non-significant
improvements in inspiratory pressure were found in 11 studies, and non-significant increase in
respiratory muscle endurance in 9 studies. Madsen used a quasi-experimental design with blinded
evaluation and found no significant changes in exercise capacity, although increases in
inspiratory muscle pressure could not be achieved808. The requirement of an adequate training
stimulus for improving dyspnoea and functional exercise capacity is acknowledged809,810, and
more recent meta-analysis concluded that IMT alone or in combination with general exercise
training decreases dyspnoea and improves exercise function in people with COPD811. The
longevity of these improvements has been shown after twelve weeks of IMT, but declined
gradually over the year if the training was not maintained812.
801
Estenne M, Knoop C, Vanvaerenbergh J, Heilporn A, de Troyer A. The effect of pectoralis muscle
training in tetraplegic subjects. Am Rev Respir Dis 1989; 139:1218-1222
802
Keens GT, Krastins IRB, Wannamaker EM, Levison H, et al. Ventilatory muscle endurance training in
normal subjects and patients with cystic fibrosis. Am Rev Respir Dis 1977; 116:853-860
803
Newell SZ, McKenzie DK, Gandevia SC. Inspiratory and skeletal muscle strength and endurance and
diaphragmatic activation in patients with chronic airflow limitation. Thorax 1989; 44:903-912
804
Leith DE, Bradley M. Ventilatory muscle strength and endurance training. J Appl Physiol 1976; 41:508516
805
Bradley ME, Leith DE. Ventilatory muscle training and the oxygen cost of sustained hyperpnea. J Appl
Physiol 1978; 45:885-892
806
Belman MJ, Mittman C. Ventilatory muscle training improves exercise capacity in chronic obstructive
pulmonary disease patients. Am Rev Respir Dis 1980; 121:273-280
807
Smith K. Respiratory muscle training in chronic airflow limitation: a meta-analysis. Am Rev Respir Dis
1992; 145:533-539
808
Madsen F, Secher NH, Kay L, et al. Inspiratory resistance versus general physical training in patients
with chronic obstructive pulmonary disease. Eur J Respir Dis 1985; 67:167-176
809
Weiner P, Berar-Yannay N, Davidovich A, et al. The cumulative effect of long acting bronchodilators,
exercise and inspiratory muscle training on the perception of dyspnoea in patients with COPD. Chest 2000;
118:672-678
810
Kim A, Larsen J, Covey M, Vitalo CA, et al. Inspiratory muscle training in patients with chronic
obstructive pulmonary disease. Nurs Res 1993; 42:356-362
811
Lötters F, Va Tol B, Kwakkel G, Gosselink R. Effects of controlled inspiratory muscle training in
patients with COPD: a meta-analysis. Eur Respir J 2002; 20:570-576
812
Weiner P, Magadle R, Beckerman M, et al. Maintenance of inspiratory muscle training in COPD
patients: one year follow-up. Eur Respir J 2004; 23:61-65
102
When adequate IMT stimulus is used, along with significant increase in respiratory muscle
endurance or strength, better maximal exercise capacity has been shown inconsistently813,814,815,816.
In addition to exercise performance, changes in dyspnoea rating can be demonstrated, without
change in HRQoL817,818. Changes in dyspnoea correlated with changes in inspiratory muscle
pressure819,820. A systematic review of IMT, using 6MWT as the outcome measure, found 8
analysable studies (6 of them being RCTs) with variable levels of methodological quality but
almost uniform improvements in 6-MWD, as long as high levels of inspiratory effort was
achieved (30% of maximum inspiratory pressure). In some studies reduced dyspnoea, better
quality of life, and improvements in both strength and endurance of inspiratory muscles were
demonstrated821. IMT conducted at home, in a study of 20 consecutive Italian COPD patients,
showed significant dyspnoea reduction and 6-MWD improvement822.
IMT may have incremental benefit over general exercise training alone823,824,825,826,827. In a RCT of
interval training with threshold loading, significant improvements were found in inspiratory
muscle pressures, respiratory muscle endurance, dyspnoea on questionnaire, and Borg-scale
813
Pardy RL, Rivington RN, Despas PJ, Macklem PT. Inspiratory muscle training compared with
physiotherapy in patients with chronic airflow limitation. Am Rev Respir Dis 1981; 123:421-425
814
Larson JL, Kim MJ, Sharp JT, Larson DA. Inspiratory muscle training with a pressure threshold
breathing device in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1988;
138:689-696
815
Guyatt G, Keller J, Singer J, et al. Controlled trial of respiratory muscle training in chronic airflow
limitation. Thorax 1992; 47:598-602
816
Preuser BA, Winningham ML, Clanton TL. High- vs low-intensity inspiratory muscle interval training
in patients with COPD. Chest 1994; 106:110-117
817
Larson JL, Kim MJ, Sharp JT, Larson DA. Inspiratory muscle training with a pressure threshold
breathing device in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1988;
138:689-696
818
Guyatt G, Keller J, Singer J, et al. Controlled trial of respiratory muscle training in chronic airflow
limitation. Thorax 1992; 47:598-602
819
Harver A, Mahler DA, Daubenspeck JA. Targeted inspiratory muscle training improves respiratory
muscle function and reduces dyspnea in patients with chronic obstructive pulmonary disease. Ann Intern
Med 1989; 111:117-124
820
Lisboa C, Munoz V, Beroiza T, et al. Inspiratory muscle training in chronic airflow limitation:
comparison of two different training loads with a threshold device. Eur Respir J 1994; 7:1266-1274
821
Tay YL, Chiang JR, Tan ML, et al. A systematic review: Effects of inspiratory muscle training on the
exercise tolerance (using the 6 minute walk test) of stage II-III COPD patients. Physio Sing 2007; 10:2-14
822
Battaglia E, Fulgenzi A, Bernucci S, et al. Home respiratory muscle training in patients with chronic
obstructive pulmonary disease. Respirology 2006; 11:799-804
823
Dekhuijzen PN, Folgering HTM, van Herwaarden CLA. Target-flow inspiratory muscle training during
pulmonary rehabilitation in patients with COPD. Chest 1991; 99:128-133
824
Weiner P, Azgard Y, Ganam R. Inspiratory muscle training combined with general exercise
reconditioning in patients with COPD. Chest 1992; 102:1351-1356
825
Wanke T, Formanek D, Lahrmann H, Merkle M, et al. Effects of combined inspiratory muscle and cycle
ergometer training on exercise performance in patients with COPD. Eur Respir J 1994; 7:2205-2211
826
Chen HI, Dukes R, Martin BJ. Inspiratory muscle training in patients with chronic obstructive
pulmonary disease. Am, Rev Respir Dis 1985; 131:251-255
827
Berry MJ, Adair NE, Sevensky KS, et al. Inspiratory muscle training and whole-body reconditioning in
chronic obstructive pulmonary disease: a controlled randomized trial. Am J Respir Crit Care Med 1996;
153:1812-1816
103
dyspnoea during activities828. Another double-blind RCT of target-flow IMT conducted at home
(10 patients in each group) showed better dyspnoea scores and HRQoL at 6 months in the
treatment group than in the controls, and shuttle walk test improvements over baseline in the
treatment group, but no change in general exercise performance829. In spite of increased
inspiratory muscle strength from IMT, however, no added benefit over home-based exercise
training could be demonstrated on exercise capacity or exercise-related symptoms830. A small
RCT comparing a resistance breathing device with “sham training” (incentive spirometry),
showed training effects in both groups, with greater increase in inspiratory muscle endurance in
patients treated with resistance muscle endurance training. There were no differences between the
two groups in dyspnoea scores, exercise capacity or HRQoL831. In a RCT involving 17 patients
with moderate-severe COPD undertaking sham training compared to 16 doing IMT at maximum
tolerable threshold load for 8 weeks (three times weekly), and significant differences were seen
between the two groups in maximum inspiratory pressure, 6-MWD, and quality of life (CRDQ,
including dyspnoea)832. IMT in asthma has been inadequately studied833.
It is remarkable that there have been five meta-analyses with systematic reviews addressing IMT.
Little evidence for benefit was found in a meta-analysis of 17 studies834. Later, a further 10
studies were analysed, showing significant improvements in inspiratory muscle strength and
endurance, with less dyspneoa during exercise835. Different levels of IMT were valuated in a third
review, and various benefits including dyspnoea and exercise capacity were found836. All these
compared IMT with sham or control. A fourth systematic review evaluated studies of IMT versus
other rehabilitation interventions, and showed added benefits from IMT for inspiratory muscle
function but not for overall exercise capacity837. The most recent systematic review reviewed 156
publications, yielding 18 RCTs of IMT with or without rehabilitation against rehabilitation.
Fourteen meta-analyses were possible, and consistent benefits in ventilatory muscle function and
in exercise capacity were demonstrated where IMT was part of the program838.
828
Covey MK, Larson JL, Wirtz SE, et al. High-intensity inspiratory muscle training in patients with
chronic obstructive pulmonary disease and severely reduced function. J Cardiopulm Rehabil 2001; 21:231240
829
Riera HS, Rubio TM, Ruiz FO, Ramos PC, et al. Inspiratory muscle training in patients with COPD.
Effect on dyspnoea, exercise performance, and quality of life. Chest 2001; 120:748-756
830
Larson JL, Covey MK, Wirtz SE, Berry JK, et al. Cycle ergometer and inspiratory muscle training in
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999; 160:500-507
831
Scherer TA, Spengler CM, Owassapian D, et al. Respiratory muscle endurance training in chronic
obstructive pulmonary disease. Am J Respir Crit Care Med 2000; 162:1709-1714
832
Hill K, Jenkins SC, Phillippe DL, Cecins N, et al. High-intensity inspiratory muscle training in COPD.
Eur Respir J 2006; 27:1119-1128
833
Ram FSF, Wellington SR, Barnes NC. Inspiratory muscle training for asthma. Cochrane Database Syst
Rev 2004; Issue 4
834
Smith K, Cook D, Guyatt GH, Madhaven J, Oxman AD. Respiratory muscle training in chronic airflow
limitation: a meta-analysis. Am Rev Respir Dis 1992; 145:533-539
835
Lotters F, van Tol B, Kwakkel G, Gosselink R. Effects of controlled inspiratory muscle training in
patients with COPD: a meta-analysis. Eur Respir J 2002; 20:570-576
836
Geddes EL, Reid WD, Crowe J, O’Brien K, Brooks D. Inspiratory muscle training in adults with chronic
obstructive pulmonary disease: a systematic review. Respir Med 2005; 99:1440-1458
837
Crowe J, Reid WD, Geddes L, O’Brien K, Brooks D. Inspiratory muscle training compared with other
rehailitation interventions in adults with chronic obstructive pulmonary disease. COPD: J COPD 2005;
3:319-329
838
O’Brien K, Geddes EL, Reid WD, Brooks D, Crowe J. Inspiratory muscle training compared with other
rehabilitation interventions in chronic obstructive pulmonary disease. A systematic review update. J
CardioPulm Rehabil Prevent 2008; 28:128-141
104
EXERCISE TRAINING
KEY POINTS
1)
Exercise training is highly effective in enhancing exercise
capacity and everyday function
2)
General physical training improves fitness
3)
Specific muscle training improves function of those muscles
4)
Upper limb training is as effective in improving respiratory
muscle function as inspiratory muscle training
5)
Strength training of muscle groups improves their strength
and may improve functional fitness
6)
Targeted inspiratory muscle training adds benefit to standard
pulmonary rehabilitation exercises
Enhancement of training with drugs, gas mixtures and
ventilation support
In a recent review of methods for modulating dynamic hyperinflation in COPD, Casaburi and
Porszasz839 suggest that this can be achieved by increasing the time available for lung emptying
or by increasing potential expiratory flow. The latter might be achieved through bronchodilator
administration or by using low density gas mixtures. The former might be achieved by exercise
training or by administration of hyeroxic gas mixtures to reduce ventilatory drive. The authors
highlighted the potential value in combining a variety of these methods.
Drug Treatment
A systematic review has collated and analysed the evidence for drug therapies improving
functional exercise capacity, though the amounts of change in performance were variable and
significant effects were described in only half of the studies 840. Until recently, there were
inadequate explanations for these improvements. Short-acting beta-agonists (e.g. salbutamol and
terbutaline) and anticholinergics (ipratropium in Australia) have only small measurable benefits
in terms of FEV1, and the duration of any benefits is fairly short. Longer acting bronchodilating
agents have only recently emerged for use in COPD, notably long-acting beta-agonists (LABA)
like salmeterol and eformoterol and the long-acting anticholinergic, tiotropium.
839
Casaburi R, Porszasz J. Reduction of hyperinflation by pharmacologic and other interventions. Proc Am
Thorac Soc 2006; 3:185-189
840
Liesker JJW, Wijkstra PJ, Koeter GH, ET AL. A systematic review of the effects of bronchodilators on
exercise capacity in patients with COPD. Chest 2002; 121:597-608
105
Tiotropium has prolonged activity at the M3 muscarinic receptor on bronchial smooth muscle841,
and has been shown to sustain significant bronchodilatation and relief of dyspnoea842,843. The
concept of dynamic hyperinflation and its reduction with therapy may provide some explanation
for functional improvements, and this hypothesis has been tested with tiotropium844. The multicentre 6-week study included 197 patients with moderately severe COPD with demonstrated
resting hyperinflation, who performed an initial maximum exercise test (cycle ergometry) to
obtain VO2max. They then performed baseline endurance tests on the cycle ergometer set at 75%
of their VO2max, and subsequent repeat endurance tests while taking tiotropium. There were
improvements in FEV1 and FVC, reduction in resting hyperinflation, and significant (mean 21%)
improvements in endurance time and exertional dyspnoea (by Borg score) at specific times in the
tests. These changes were supported by significant improvements in daily dyspnoea measured by
BDI/TDI.
Most recently, positive interaction between tiotropium and pulmonary rehabilitation has been
examined, based on the premise that, if the drug has the properties demonstrated above, it should
allow the patient to undertake more work and therefore gain more benefit from the PR845. In fact,
this 25-week study demonstrated significant enhancement of the benefits from PR. In a multicentre design 108 patients were randomised to tiotropium or placebo, which they took for 5
weeks before starting a minimum of eight weeks of thrice-weekly lower-limb targeted endurance
exercise training and continuing tiotropium throughout. Maintenance of benefit effects were also
examined 12 weeks after PR was completed and the drug had been continued. Tiotropium alone
was better than placebo at increasing constant-work treadmill endurance tests (at 80% of
maximum work achieved in a maximal incremental treadmill tests pre-treatment) – over the first
4 weeks the difference was 1.65 minutes (p=0.183). Following PR in addition to tiotropium or
placebo there were significant improvements in endurance time in both groups, but tiotropium
patients had significantly greater benefit from PR (by 5.35 mins, p=0.025), and the benefit was
sustained 12 weeks later (difference + 6.60 mins, p=0.018). TDI dyspnoea improved more in the
tiotropium group at all time-points (by clinically-meaningful margins), as did health-related
quality of life (SGRQ – by a margin of 4.44 units) (p=0.055)846.
Work is being done with LABA to determine if similar effects can be replicated with a different
class of long-acting drugs. If it can be shown that combinations of different classes had at least
additive benefits, it might be feasible to utilise these effects to enhance training.
Oxygen
The primary rationale for the use of oxygen in hypoxaemic patients with COPD is to prolong
life847, and there are concomitant benefits in reducing pulmonary artery pressure (which
841
Disse B. Antimuscarinic treatment for lung diseases from research to clinical practice. Life Sci 2001;
68:2257-2564
842
Casaburi R, Mahler DA, Jones PW, et al. A long-term evaluation of once-daily inhaled tiotropium in
chronic obstructive pulmonary disease. Eur Respir Dis 2002; 19:217-224
843
Vincken W, van Noord JA, Greethorst APM, et al. Improved health outcomes in patients with COPD
during 1 yr’s treatment with tiotropium. Eur Respir J 2004; 23:832-840
844
O’Donnell DE, Fluge T, Gerken F, Hamilton A, et al. Effects of tiotropium on lung hyperinflation,
dyspnoea and exercise tolerance in COPD. Eur Respir J 2004; 23:832-840
845
Casaburi R, Kukafka D, Cooper CB, ET AL. Improvement in exercise tolerance with the combination of
tiotropium and pulmonary rehabilitation in patients with COPD. Chest 2005; 127:809-817
846
Casaburi R, Kukafka D, Cooper CB, ET AL. Improvement in exercise tolerance with the combination of
tiotropium and pulmonary rehabilitation in patients with COPD. Chest 2005; 127:809-817
847
Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic
obstructive lung disease. Ann Intern Med 1980; 93:391-398
106
contributes to the improved survival)848. Intermittent short bursts of oxygen to avoid or reduce
dyspnoea during exercise has little documented evidence in patients with COPD who do not have
significant hypoxaemia849,850,851,852. On the other hand, in non-hypoxaemic patients, as well as
those with hypoxaemia, hyperoxic mixtures have been shown to reduce dyspnoea, attributed to
reduced tidal volume and reduced dynamic hyperinflation853. Whether this is due to the oxygen
per se, or to an effect of gas-driven positive end expiratory pressure (PEEP) from the oxygen
mask854 is still speculative, but dynamic hyperinflation is an important cause of dyspnoea in
people with COPD855. There are further inconsistencies in evidence supporting use of oxygen.
Neither oxygen supplementation nor air, provided either before or after exercise in a randomorder double-blind study had significant effect on exercise-induced dyspnoea, exercise endurance
or recovery time in 52 patients with severe COPD who had previously desaturated during a 6minute walk test856. In another study of 30 non-hypoxaemic patients with less severe COPD a
double-blind trial with air or oxygen at 3LPM was undertaken. The patients used the test gas
during exercise training on a cycle ergometer 3 times a week for 7 weeks. Greater training effects
were seen in the group receiving oxygen than in those receiving air, with greater endurance and
reduced ventilation and dyspnoea at isotime857, but it is important to note that this applied to high
intensity exercise training (as recommended from the studies by Casaburi858). The reduced
ventilation would have contributed to reduced dynamic hyperinflation (though this was not
measured in that study), as shown in subsequent studies859,860,861. Administration of 100% oxygen
(rather impractical in everyday circumstances) can enhance work by relieving skeletal muscles of
metabolic demand862, and this could allow greater muscle conditioning.
848
Ashutosh K, Mead G, Demsky M. Early effects of oxygen administration and prognosis in chronic
obstructive pulmonary disease and cor pulmonale. Am Rev Respir Dis 1983; 127:399-404
849
Evans TW, Waterhouse JC, Carter A, et al. Short burst oxygen treatment for breathlessness in chronic
obstructive airways disease. Thorax 1986; 41:611-615
850
McKeon JL, Murree-Allen K, Saunders NA. Effects of breathing supplemental oxygen before
progressive exercise in patients with chronic obstructive lung disease. Thorax 1988; 43:53-56
851
Stevenson NJ, Calverley PMA. The effects of oxygen on resolution of breathlessness after exercise. Am
J Respir Crit Care Med 2002; 165:A264
852
Lewis CA, Eaton TE, Young P, Kolbe J. Short-burst oxygen immediately before and after exercise is
ineffective in nonhypoxic COPD patients. Eur Respir J 2003; 22:584-588
853
Alvisi V, Mirkovic T, Nesme P, et al. Acute effects of hyperoxia on dyspnea in hypoxemic patients with
chronic airway obstruction at rest. Chest 2003; 123:1038-1046
854
Bellemare F, Grassino A. Force reserve of the diaphragm in patients with chronic obstructive pulmonary
disease. J Appl Physiol 1983; 55:8-15
855
Eltayara L, Becklake MR, Volta CA, et al. Relationship between chronic dyspnea and expiratory flow
limitation in COPD patients. Am J Respir Crit Care Med 1996; 154:1726-1734
856
Nandi K, Smith AA, Crawford A, MacRae KD, et al. Oxygen supplementation before or after
submaximal exercise in patients with chronic obstructive pulmonary disease. Thorax 2003; 58:670-673
857
Emtner M, Porszasz J, Burns J, et al. Benefits of supplemental oxygen in exercise training in
nonhypoxemic chronic obstructive pulmonary disease patients. Am J Respir Crit Care Med 2003;
168:1034-1042
858
Casaburi R, Patessio A, Ioli F, et al. Reductions in exercise lactic acidosis and ventilation as a result of
exercise training in patients with obstructive lung disease. Am Rev Respir Dis 1991; 143:9-18
859
O’Donnell DE, D’Arsigny C, Webb KA. Effects of hyperoxia on ventilatory limitation during exercise
in advanced chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001; 163:892-898
860
O’Donnell DE, Bain DJ, Webb KA. Factors contributing to relief of exertional breathlessness during
hyperoxia in chronic airflow limitation. Am J Respir Crit Care Med 1997; 155:530-535
861
Somfay A, Porszasz J, Lee SM, Casaburi R. Dose-response effect of oxygen on hyperinflation and
exercise endurance in nonhypoxemic COPD patients. Eur Respir J 2001; 18:77-84
862
Richardson RS, Sheldon J, Poole DC, Hopkins SR, et al. Evidence of skeletal muscle metabolic reserve
during wholebody exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care
Med 1999; 159:881-885
107
A recent systematic review that evaluated effects of ambulatory oxygen during exercise compared
to placebo included 31 randomised controlled trials involving 534 patients with moderate and
severe COPD863. Oxygen treatment significantly improved outcomes related to exercise capacity
(maximal and endurance) as well as dyspnoea at isotime of endurance exercise. More specific to
exercise training, however, is another recent systematic review which addressed RCTs comparing
exercise training with oxygen supplement vs non-supplemented training for patients with COPD
not using home oxygen therapy864. Five RCTs matched the inclusion criteria, with only three
being included in meta-analysis, providing only 31 treated patients and 32 controls, and there
were suboptimal quality issues. The authors found insufficient evidence supporting oxygen
supplementation during exercise training and recommended better-constructed trials evaluating
relevant patient-centred outcomes.
Heliox
There is some attraction to the notion that giving people with severe COPD a gas mixture that is
less dense to breathe would reduce dyspnoea. If airways conduct air with turbulent flow, there
should be significant improvement in flow with the less-dense gas865. Since a mixture of helium
with oxygen was introduced by Barach in 1934866 to reduce dyspnoea in asthma, emphysema and
upper airways obstruction, there have been sporadic research reports of its therapeutic use.
Ventilatory responses to incremental cycle ergometry exercise in 12 older healthy (and fit) people
were increased when they breathed heliox867. An experiment with a mixture of 80% helium with
20% oxygen (heliox) did not change tidal flow limitation, and did not reduce dynamic
hyperinflation868. In another study of 12 people with COPD endurance time was higher and
dynamic hyperinflation less when they exercised to exhaustion while breathing heliox than when
breathing room air, despite heliox increasing ventilatory responses to exercise869. These patients
reported less dyspnoea at isotime, and the reduction in dyspnoea correlated with the increase in
inspiratory capacity (IC). In a further study, the La Jolla group found that whole body exercise
(cycling) by people with COPD was enhanced by heliox breathing due to increased muscle
metabolic reserve870. Interestingly, though, the better exercise tolerance experienced during heliox
breathing was not translated into better training benefits in another study871. Properly designed
randomised controlled trials with double-blinding are therefore warranted, though this is difficult,
given the different density, visco-elastic properties and thermal conductivity of helium, and hence
likelihood of subjects being aware of which gas mixture is being breathed. Furthermore, it may be
interesting to examine whether heliox would enhance exercise training, and secondly whether use
863
Bradley JM, O’Neill B. Short-term ambulatory oxygen for chronic obstructive pulmonary disease.
Cochrane Database Syst Rev 2006; Issue 4
864
Nonoyama ML, Brooks D, Lacasse Y, et al. Cochrane Database Syst Rev 2007 ; Issue 2 : CD005372
865
GrapГ© B, Channin E, Tyler JM. The effect of helium and oxygen mixtures on pulmonary resistances in
emphysema. Am Rev Respir Dis 1960; 81:823-829
866
Barach AL. Use of helium as a new therapeutic gas. Proc Soc Exp Biol Med 1934; 32:462
867
Babb TG, DeLorey DS, Wyrick BL. Ventilatory responses to exercise in aged runners breathing He-O2
or inspired CO2. J Appl Physiol 2003; 94:685-693
868
Pecchiari M, Pelucchi A, D’Angelo E, Foresi A, et al. Effect of heliox breathing on dynamic
hyperinflation in COPD patients. Chest 2004; 125:2075-2082
869
Palange P, Valli G, Onorati P, Antonucci R, et al. Effect of heliox on lung dynamic hyperinflation,
dyspnea, and exercise endurance capacity in COPD patients. J Appl Physiol 2004; 97:1637-1642
870
Richardson RS, Sheldon J, Poole DC, Hopkins SR, et al. Evidence of skeletal muscle metabolic reserve
during wholebody exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care
Med 1999; 159:881-885
871
Johnson JE, Gavin DJ, Adams-Dramiga S. Effects of training with heliox and noninvasive positive
pressure ventilation on exercise ability in patients with severe COPD. Chest 2002; 122:464-472
108
of a more hyperoxic mixture with helium would unload ventilation and work of breathing to
allow greater training effects than hyperoxia alone.
Another therapeutic option is to combine helium gas with a hyperoxic mixture. In a double-blind
randomised cross-over design, such a mixture has been shown superior to either hyperoxia (28%
oxygen) or standard heliox (21% oxygen) in endurance shuttle walk distance872, a finding that
elsewhere was determined to be due to reduced DH and reduced respiratory rate873,874.
Applicability of this modality to the rehabilitation setting requires further evaluation. Helium is a
limited resource that is increasingly costly, and a health economic evaluation is warranted.
Ventilation support
Non-invasive positive pressure ventilation (NPPV) has been suggested as another way of
supporting ventilation to enhance training. This strategy is known to increase ventilation and
reduce dyspnoea875, with reduced inspiratory effort876 and ventilatory loading877. There is some
inconsistency in the evidence again that this may allow better training effects from pulmonary
rehabilitation878,879,880. Recent evidence suggests this difficult strategy provides little or no benefit
in enhancing training881, even though higher pressures can enhance endurance882.
Education
The education component “should be part of the care for every patient with COPD”883, and “all
patients may benefit from fuller explanation of the disease processes, the effects of treatment,
872
Laude EA, Duffy NC, Baveystock C, Dougill B, Campbell MJ, Lawson R, et al. The effect of helium
and oxygen on exercise performance in chronic obstructive pulmonary disease: a randomized crossover
trial. Am J Respir Crit Care Med 2006; 173:865-870
873
Eves ND, Petersen SR, Haykowsky MJ, Wong EY, Jones RJ. Helium-hyperoxia, exercise, and
respiratory mechanics in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2006;
174:763-771
874
Marciniuk DD, Butcher SJ, Reid JK, Macdonald GF, Eves ND, Clemens R, et al. The effects of heliumhyperoxia on 6-minute walking distance in chronic obstructive pulmonary disease: a randomized,
controlled trial. Chest 2007; 131:1659-1665
875
Maltais F, Reissman H, Gottfried SB. Pressure support reduces inspiratory effort and dyspnoea during
exercise in chronic airflow obstruction. Am J Respir Crit Care Med 1995; 151:1027-1033
876
Kyroussis D, Polkey MI, Hamnegard C-H, Mills GH, et al. Respiratory muscle activity in patients with
COPD walking to exhaustion with and without pressure support. Eur Respir J 2000; 15:649-655
877
Polkey MI, Kyroussis D, Mills GH, et al. Inspiratory pressure support reduces slowing of inspiratory
muscle relaxation rate during exhaustive treadmill walking in severe COPD. Am J Respir Crit Care Med
1996; 154:1146-1150
878
Bianchi L, Foglio K, Pagani M, Vitacca M, et al. Effects of proportional assist ventilation on exercise
tolerance in COPD patients with chronic hypercapnia. Eur Respir J 1998; 11:422-427
879
Dolmage TE, Goldstein RS. Proportional assist ventilation and exercise tolerance in subjects with
COPD. Chest 1997; 111:948-954
880
Johnson JE, Gavin DJ, Adams-Dramiga S. Effects of training with heliox and noninvasive positive
pressure ventilation on exercise ability in patients with severe COPD. Chest 2002; 122:464-472
881
Highcock MP, Shneerson JM, Smith IE. Increased ventilation with NiIPPV does not necessarily
improve exercise capacity in COPD. Eur Respir J 2003; 22:100-105
882
van’t Hul A, Gosselink R, Hollander P, et al. Acute effects of inspiratory pressure support during
exercise in patients with COPD. Eur Respir J 2004; 23:34-40
883
American Thoracic Society Official Statement. Standards for the Diagnosis and Care of Patients with
Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med 1995; 152:S77-S120
109
how and when to use inhalers, and when to ask for help”884. The NICE (UK) guidelines for
COPD management state that “..education is usually offered as part of a comprehensive
pulmonary rehabilitation programme…[despite] little robust evidence relating to COPD patient
education”885.
American guidelines for pulmonary rehabilitation886 consider education as “psychosocial
intervention components”, and propose four interventions – psychosocial, health behaviour,
adherence, and education. Psychosocial interventions include stress management (which has
small effects on the Sickness Impact Profile887), progressive muscle relaxation (which has small
and brief effects on anxiety and breathlessness888,889), and yoga (which in a single randomised
trial showed increased exercise performance and reduced symptoms890). Smoking cessation and
nutrition management are included in health behaviour interventions. Attention to smoking
cessation has been studied in people with COPD, showing modest results with a variety of
interventions891,892,893. A systematic review concluded that combined pharmacological and
behavioural interventions are better than no intervention or psychosocial intervention in
supporting smoking cessation in COPD, and can be effective, though the strength of this evidence
was poor894. and there are no studies of behavioural weight management in COPD. Other
behavioural strategies were moderately cost-effective in a small randomised controlled trial895.
Adherence to smoking cessation, exercise regimens and prescribed medications are central to
good COPD management896. Adherence to smoking cessation is a complex issue, both in the
884
British Thoracic Society Standards of Care Subcommittee on Pulmonary Rehabilitation. Pulmonary
rehabilitation. Thorax 2001; 56:827-834
885
The National Collaborating Centre for Chronic Conditions. Chronic obstructive pulmonary disease.
National clinical guidelines on management of chronic obstructive pulmonary disease in adults in primary
and secondary care. Thorax 2004; 59 (Suppl I):1-232
886
AACVPR/ACCP Pulmonary Rehabilitation Guidelines Panel. Pulmonary Rehabilitation. Joint
ACCP/AACVPR evidence-based guidelines. Chest 1997; 112:1363-1396
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Blake RL, Vandiver TA, Braun S, Bertuso DD, Straub V. A randomized controlled evaluation of a
psychosocial intervention in adults with chronic lung disease. Fam Med 1990; 22:365-370
888
Renfroe KL. Effect of progressive relaxation on dyspnoea and state anxiety in patients with chronic
obstructive pulmonary disease. Heart Lung 1988; 17:408-413
889
Gift AG, Moore T, Soeken K. Relaxation to reduce dyspnoea and anxiety in COPD patients. Nurs Res
1992; 41:242-246
890
Tandon MK. Adjunct treatment with yoga in chronic severe airways obstruction. Thorax 1978; 33:514517
891
Turner SA, Daniels JL, Hollandsworth JG. The effects of a multicomponent smoking cessation program
with chronic obstructive pulmonary disease outpatients. Addict Behav 1985; 10:87-90
892
Buist AS, Connett JE, Miller RD, Kanner RE, et al. Chronic Obstructive Pulmonary Disease Early
Intervention Trial (Lung Health Study). Baseline characteristics of a randomized population. Chest 1993;
103:1863-1872
893
Pedersen LL, Wanklin JM, Lefcoe NM. The effects of counseling on smoking cessation among patients
hospitalized with chronic obstructive pulmonary disease: a randomized clinical trial. Int J Addict 1991;
26:107-119
894
van der Meer RM, Wagena EJ, Ostelo RWJG, et al. Smoking cessation for chronic obstructive
pulmonary disease. Cochrane Database Syst Rev 2006; Issue 4
895
Toevs CD, Kaplan RM, Atkins CJ. The costs and effects of behavioral programs in chronic obstructive
pulmonary disease. Med Care 1984; 22:108-110
896
Eakin EG, Sassi-Dombron D, Kaplan RM, Ries AL. Clinical trial of rehabilitation in chronic obstructive
pulmonary disease: Compliance as a mediator of change in exercise endurance. J Cardiopulm Rehabil
1992; 12:105-110
110
short term897 and long term898. Yet fully half the people in a large US survey who had ever
smoked were not smoking at the time of survey, suggesting self-regulation is often eventually
successful899. Methods for improving sustained abstinence are considered elsewhere.
Nonadherence to treatment covers two major components. Primary nonadherence refers to the
patient not filling or collecting a prescription, either due to cost limitations or to poor
understanding900. Secondary nonadherence refers to the medication being used incorrectly or
being prematurely stopped, often due to adverse effects, belief the benefit has been achieved and
no more is required, or fear of accumulated “resistance” with repeated use901. Fear of adverse
effects particularly relates to use of corticosteroids902. Of course, inhaled medications require use
of sometimes seemingly complex devices, and often several different forms of device.
Recognition of the importance of this factor has been highlighted by publication by the American
College of Chest Physicians of guidelines for clinicians in selecting and educating patients about
inhalation device use903. Frequency of prescribed use is an important factor, and once-daily
medication determines higher adherence than the need for multiple daily doses904. Oxygen
therapy also is affected by adherence issues, with a similar set of perceptions and difficulties
being identifiable905, and specific education relating to the use of oxygen equipment improves
adherence906.
Despite abundant evidence for the benefits of exercise-centred pulmonary rehabilitation, there is
almost equally abundant evidence that many patients fail to attend courses (1% in Australia and
New Zealand, 3% in Belgium). Reluctance to take responsibility, and access difficulties are
frequently identified reasons. Further, not all who attend achieve significant improvements in
exercise performance – perhaps as many as a third fail to improve907, although this does not
appear to be determined by disease severity908. A randomised controlled study of cognitive and
behavioural interventions showed people with COPD who received combined cognitivebehavioural interventions continued exercise more than those assigned to behaviour modification
897
Hughes JR, Keely J, Naud S. Shape of the relapse curve and long-term abstinence among untreated
smokers. Addiction 2004; 99:29-38
898
Anthonisen NR, Connett JE, Murray RP. Smoking and lung function of Lung Health Study participants
after 11 years. Am J Respir Crit Care Med 2002; 166:675-679
899
Maurice E, Trosclair A, Merritt R, et al for the Office on Smoking and Health, National Center for
Chronic Disease Prevention and Health Promotion, CDC. Cigarette smoking among adults – United States,
2004. MMWR Morb Mortal Weekly Rep 2005; 54: 1121-1124
900
Pierre JD, Heisler M, Wagner TH. Cost-related medication underuse: do patients with chronic illness tell
their doctor? Arch Intern Med 2004; 164:1749-1755
901
Rand CS. Patient adherence with COPD therapy. Eur Respir Rev 2005;14:97-101
902
Jones RCM, Hyland ME, Hanney K, Erwin J. A qualitative study of compliance with medeication and
lifestyle modification in chronic obstructive pulmonary disease (COPD). Prim Care Respir J 2004; 13:149154
903
Dolovich MB, Ahrens RC, Hess DR, et al. Device selection and outcomes of aerosol therapy: evidencebased guidelines. Chest 2005; 127:335-371
904
Kruk ME, Schwalbe N. The relation between intermittent dosing and adherence: Preliminary insights.
Clin Ther 2006; 28:1989-1995
905
Kampelmacher MJ, van Kesteren RG, Alsbach GPJ, et al. Characteristics and complaints of patients
prescribed long term oxygen therapy in the Netherlands. Respir Med 1998; 92:70-75
906
Peckham DG, McGibbon K, Tonkinson J, et al. Improvement in patient compliance with long term
oxygen therapy following formal assessment with training. Respir Med 1998; 92:1203-1206
907
Troosters T, Gosselink R, Decramer M. Exercise training in COPD: how to distinguish responders from
nonresponders. J Cardiopulm Rehabil 2001; 21:10-17
908
Berry MJ, Rejeski WJ, Adair NE, Zaccaro D. Exercise rehabilitation and chronic obstructive pulmonary
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111
or cognitive modification, and all treatments were more effective than controls. Benefits were lost
by 6 months, however909. More recent work evaluated 103 patients with COPD who were
randomly assigned to one of three types of dyspneoa self-management. Consistent adherence to
the exercise prescribed resulted in greatest improvements in physical function910.
Modest health gains can be expected from knowledge education for people with COPD,
depending on the aim of the education input, and expert panels agree that education should be
combined with other components of pulmonary rehabilitation, with emphasis on acquiring
relevant techniques and skills, as well as adherence and self-management911,912.
FIGURE 4.5
EDUCATION SHOULD INCLUDE SOME UNDERSTANDING OF RESPIRATORY
FUNCTION, AS WELL AS TRAINING DEVOTED TO SKILLS ACQUISTION
The approach to education influences the level of benefit. Early attempts with group therapy to
teach post-myocardial infarction patients about the disease and required treatment, for example,
909
Atkins CJ, Kaplan RM, Timms RM, Reinsch S, Lofback K. Behavioral exercise programs in the
management of chronic obstructive pulmonary disease. J Consult Clin Psychol 1984; 52:591-603
910
Donesky-Cuenco D-A, Janson S, Neuhaus J, Neilands TB, Caerrieri-Kahlman V. Adherence to a homewalking prescription in patients with chronic obstructive pulmonary disease. Heart Lung 2007; 36:348-363
911
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary
Disease. Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report.
National Institutes of Health; NHLBI Publication Number 2701. April 2001
912
National Collaborating Centre for Chronic Conditions. Chronic obstructive pulmonary disease. National
clinical guideline on management of chronic obstructive pulmonary disease in adults in primary and
secondary care. Thorax 2004; 59 (Suppl 1):1-232
112
were found to increase patient anxiety913, and enforced analysis of the patient’s personality and
psychological defences was not helpful914. Provision of written educational materials might be
the simplest approach to giving people facts, but a systematic review of the efficacy of such a
passive approach for health care workers (eleven studies involving 1,848 physicians) found
equivocal results for change in practice915. No such research into passive education for patients
has been identified. However, simple teaching about a patient’s lung disease can improve
knowledge, and may be associated with reduced use of hospital and primary care facilities916. Use
of videotapes has been studied in a randomised trial in 214 patients with COPD, comparing
videotape customised to disease type and severity with standard information on videotape and
with usual care. There were statistically significant improvements in quality of life and fatigue
and better adherence to exercise in patients receiving the customised videotape than the other
interventions, and the benefits were sustained for 16 weeks’ observation917.
Guidelines recommend that there should be input from a range of health professionals working
together to improve the patient’s knowledge about breathing and the various treatments available
to control breathlessness. There is an emerging emphasis on boosting psychosocial supports, and
in particular instilling hope, and removing feelings of isolation and helplessness918,919. Fahrenfort
favours “emancipation: liberating people to make their own decisions on their own terms” 920.
Knowledge of facts, and understanding concepts that allow application of facts, are the basic
foundations of patient education. Knowledge acquisition, emphasis on the need to quit smoking,
assistance in quitting, support to maintain tobacco abstinence, optimising activities and nutrition,
enabling control over anxiety, panic or depression, and training in use of medications and
therapeutic devices to their best advantage appear relevant in chronic lung disease. Behavioural
change, though, is likely to occur only when the patient is able to identify the relevance of the
concepts to their own condition and treatment. Indeed, in COPD specific efficacy expectations in
relation to activity tasks can improve compliance with exercises and improved functional
status921.
The ATS guidelines on COPD management support a tailored approach for individual patients,
but recommends combining group discussions with education at each interaction between health
professional and patient. Education alone has limited documented benefit922,923. In asthma, for
913
Wallace N, Wallace DC. Group education after myocardial infarction: Is it effective? Med J Aust 1977;
2:245-247
914
Ibrahim MA, Feldman JG, Sultz HA, Staiman MG, et al. Management after myocardial infarction: A
controlled trial of the effect of group psychotherapy. Int J Psychiatry Med 1974; 5:253-268
915
Freemantle N, Harvey EL, Wolf F, Grimshaw JM, et al. Printed educational materials: effects of
professional practice and health care outcomes. Cochrane Database Syst Rev 2002; Issue 1.
916
Tougaard L, Krone T, Sorknaes A, Ellegaard H. Economic benefits of teaching patients with chronic
obstructive pulmonary disease about their illness. The PASTMA Group. Lancet 1992; 339:1517-1520
917
Petty TL, Dempsey EC, Collins T, Pluss W, et al. Impact of customized videotape education on quality
of life in patients with chronic obstructive pulmonary disease. J Cardiopulm Rehabil 2006; 26:112-117
918
Roback HB. Helping patients and their families with medical problems. San Francisco CA: JosseyBass; 1984.
919
Yalom ID. The theory and practice of group psychotherapy. 2nd ed. New York: Basic Books; 1985
920
Fahrenfort M. Patient emancipation by health education: an impossible goal? Patient Ed Counsel 1987;
10:25-37
921
Kaplan RM, Atkins CJ, Reinsch S. Specific efficacy expectations mediate exercise compliance in
patients with COPD. Health Psychol 1984; 3:223-242
922
Howland J, Nelson EC, Barlow PB, McHugo G, et al. Chronic obstructive airway disease: Impact of
health education. Chest 1986; 90:233-238
113
example, it is known that information-only approaches to education do not improve health care
utilisation924. For smoking cessation, simple advice, support and group therapy sessions do have a
small role925, though they are less efficacious than a more comprehensive approach926. Further
information on strategies for helping people quit smoking can be found in other texts, as
discussed above, and in two further meta-analyses927,928.
Several different types of education for COPD have been studied in one semi-controlled trial, and
improvements were seen in well-being, self-efficacy, compliance with recommended exercise
regimens and actual exercise tolerance929. This group also performed an attention-controlled
randomised trial of specific training for exercise compliance in 60 COPD patients, and confirmed
this intervention resulted in greater compliance with the exercise regimen. Few studies have
examined the effects of education-only pulmonary rehabilitation on health outcomes. There is no
significant effect on lung function or on exercise performance930,931,932. A randomised trial of
education alone versus comprehensive pulmonary rehabilitation in COPD patients was conducted
in 119 patients 933. All received small-group teaching about COPD and coping strategies, and 57
also had individual chest physiotherapy, group psychosocial support sessions and weekly exercise
training. Improvements were significantly greater with comprehensive PR than education alone
for exercise capacity and endurance, perceived breathlessness, muscle fatigue, dyspnoea and
walking self-efficacy, although these benefits slowly waned over 2 to 4 years. No differences
were seen in health economic outcomes, survival, depression or quality of life.
There is increasing interest in training patients and their carers to develop a partnership
approach to treatment with their medical mentors. With this approach they should be able to selfmonitor their disease more effectively, to adhere to medications and use them correctly, and to
manage their disease on a day-to-day basis, so preventing or limiting exacerbations. Asthma selfmanagement programs have shown generally good results in adults934,935,936 (with some
923
Make BJ. Collaborative self-management strategies for patients with respiratory disease. Respir Care
1994; 39:566-579
924
Gibson PG, Coughlan J, Wilson AJ, Hensley MJ, et al. Limited (information only) patient education
programs for adults with asthma. Cochrane Database Syst Rev 2000; (2):CD001005
925
Stead LF, Lancaster T. Group behaviour therapy programmes for smoking cessation (Cochrane
Review), in: The Cochrane Library Issue 3, 1998. Oxford: Update Software
926
Raw W, McNeill A, West R. Smoking cessation guidelines for health professionals. Thorax 1998; 53
(Suppl 5, Pt 1):S1-S19
927
Baillie AJ, Mattick RP, Hall W, Webster P. Meta-analytic review of the efficacy of smoking cessation
interventions. Drug Alcohol Rev 1994; 13:157-170
928
Kottke TE, Battista RN, DeFriese GH, Brekke ML. Attributes of successful smoking cessation
interventions in medical practice. A meta-analysis of 39 controlled studies. JAMA 1988; 259:2883-2889
929
Atkins CJ, Kaplan RM, Timms S, Reinsch S, Lofback K. Behavioral programs in the management of
chronic obstructive pulmonary disease. J Consult Clin Psychol 1984; 52:591-603
930
Janelli LM, Scherer YK, Schmeider LE. Can a pulmonary health teaching program alter patients' ability
to cope with COPD? Rehabil Nurs 1991; 16:199-202
931
Ashikaga T, Vacek PM, Lewis SO. Evaluation of a community-based education program for individuals
with chronic obstructive pulmonary disease. J Rehabil 1980; 46:23-27
932
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995;
122:823-832
933
Toshima MT, Blumberg E, Ries AL, Kaplan RM. Does rehabilitation reduce depression in patients with
chronic obstructive pulmonary disease. J Cardiopulm Rehabil 1992; 12:261-269
934
Maiman LA, Green LW, Gigson G, MacKenzie EJ. Education for self-treatment by adult asthmatics.
JAMA 1979; 241:1919-1922
114
inconsistencies937) and in children938,939,940,941. Medication compliance/adherence in asthma may
be improved by specific education942,943.
American/European guidelines for pulmonary rehabilitation now include self-management
education for COPD944. One randomised uncontrolled study in COPD patients showed that
patient education by group and individual sessions did alter patients’ medication habits, in that
less short-acting beta-agonist bronchodilator was dispensed, but there was no change in
compliance with inhaled corticosteroid use in either asthmatics or people with COPD945. HRQoL
effects were significant for asthma but not for COPD patients946. Self-management education
for people with COPD resulted in no changes in dyspnoea, but self-efficacy was found to be
better in a small quasi-experimental non-random uncontrolled study947. A non-randomised but
controlled study in people with COPD has shown improvements in self-efficacy with education
alone but not as great as they were with combined education and supervised exercise training948.
A meta-analysis of 65 studies meeting specific requirements of experimental design found few
studies of education-alone in COPD, with relatively small numbers in the studies, and small sized
effects for accuracy in performing inhaler skills, health care utilisation and adherence to
treatment949. In addition, small improvements have been demonstrated for aspects of quality of
935
Snyder SE, Winder JA, Creer TL. Development and evaluation of an adult asthma self-management
program. J Asthma 1987; 24:154-158
936
Bailey WC, Richards JM, Brooks CM, Soong SJ, et al. A randomized trial to improve self-management
practices of adults with asthma. Arch Intern Med 1990; 150:1664-1668
937
Bailey WC, Kohler CL, Richards JM, Windsor RA, et al. Asthma self-management: do patient
education programs always have an impact? Arch Intern Med 1999; 159:2422-2428
938
Clark NM, Feldman CH, Freudenberg N, Millman EJ, et al. Developing education for children with
asthma through study of self-management behavior. Health Educ Q 1980; 7:278-297
939
Bruhn JG. The application of theory in childhood asthma self-help program. J Allergy Clin Immunol
1987; 72:562-577
940
Madge P, McColl J, Paton J. Impact of a nurse-led home management training programme in children
admitted to hospital with acute asthma: a randomized controlled study. Thorax 1997; 52:223-228
941
Wesseldine L, McCarthy P, Silverman M. A structured discharge procedure for children admitted to
hospital with acute asthma: a randomized controlled trial of nursing practice. Arch Dis Child 1999; 80:110114
942
Windsor RA, Bailey WC, Richards JM, Manzella B, et al. Evaluation of the efficacy and cost
effectiveness of health education methods to increase medication adherence among adults with asthma. Am
J Publ Health 1990; 80:1519-1521
943
Allen RM, Jones MP, Oldenburg B. Randomised trial of an asthma self-management programme for
adults. Thorax 1995; 50:731-738
944
Nici L, Donner C, Wouters E, ZuWallack R, et al, on behalf of the ATS/ERS Pulmonary Rehabilitation
Writing Committee. American Thoracic Society/European Respiratory Society Statement on Pulmonary
Rehabilitation. Am J Respir Crit Care Med 2006; 173:1390-1413
945
Gallefoss F, Bakke PS. How does patient education and self-management among asthmatics and people
with chronic obstructive pulmonary disease affect medication? Am J Respir Crit Care Med 1999;
160:2000-2005
946
Gallefoss F, Bakke PS, Kjaersgaard P. Quality of life assessment after patient education in a randomized
controlled study on asthma and chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999;
159:812-817
947
Zimmerman BW, Brown ST, Bowman JM. A self-management program for chronic obstructive
pulmonary disease: relationship to dyspnoea and self-efficacy. Rehabil Nurs 1996; 21:253-257
948
Scherer YK, Schmieder LE, Shimmel S. The effects of education alone and in combination with
pulmonary rehabilitation on self-efficacy in patients with COPD. Rehabil Nurs 1998; 23:71-77
949
Devine EC, Pearcy J. Meta-analysis of the effects of psychoeducational care in adults with chronic
obstructive pulmonary disease. Patient Educ Couns 1996; 29:167-178
115
life and dyspnoea from education-alone in randomised controlled trials950,951,952. Self-management
in asthma is well established and validated, but there is still much work needed in demonstrating
effectiveness and cost-effectiveness in COPD953. A recent systematic review evaluated 17 RCTs
of self-management education by lay leaders among 7,442 participants with a range of chronic
health conditions, all but one relatively short term954. Small short-term improvements were seen
in patient self-efficacy, symptom management and frequency of programmed exercises, but no
significant changes in mental health, HRQoL, respiratory symptoms or use of healthcare
resources. The potential benefits, limitations and costs of such self-management education
programs have recently been highlighted in Australia955. Another recent systematic review
examined self-management education in general for COPD, and included 14 RCTs, though metaanalysis could not be undertaken for all outcomes because of marked heterogeneity in the
measures used and designs of trials. Reduced hospital utilization was the major outcome
identified956. Efficacy for action plans as a modality of self-management could not be identified
due to inadequate data, but a specific review has identified efficacy957.
The improvements in performance parameters seen following exercise training regimens in
people with COPD has tended to bias some professionals against the role of detailed education
programs. Rising interest in self-management for people with COPD, particularly around
exacerbations, is slowly changing these attitudes. For patients to respond to exacerbations in a
timely and appropriate way, they need to be aware of new symptoms, understand what they and
their medical care providers mean by exacerbations, and act accordingly. A recent report from a
multicentre European qualitative interview-based study of patient understanding and recognition
of exacerbations of COPD (n-125) showed poor understanding of the term exacerbation and wide
variations in symptomatology, but individuals were able to identify their own exacerbations958. A
New Zealand prospective randomised controlled trial (n=159) of structured education about use
of self-management plans that included use of courses of antibiotics and steroids for early
exacerbations detected by patients themselves found self-management knowledge was higher in
the treatment group, but there was no difference between the groups in quality of life959. Written
action plans were provided to patients with moderate to severe COPD in an Australian
prospective randomised controlled trial (n=139) showed greater use of antibiotics and steroids in
950
Rosser R, Denford J, Heslop A, Kinston W, et al. Breathlessness in and psychiatric morbidity in chronic
bronchitis and emphysema: a study of psychotherapeutic management. Psychol Med 1983; 13:93-110
951
Frith P, Walker P, Rowland S, Atkinson J. Using an education program for improving quality of life in
patients with chronic obstructive pulmonary disease. Chest 1993; 103:180S
952
Sassi-Dambron DE, Eakin EG, Ries AL, Kaplan RM. Treatment of dyspnoea in COPD: A controlled
clinical trial of dyspnoea management strategies. Chest 1995; 107:724-729
953
Bourbeau J. Disease-specific self-management programs in patients with advanced chronic obstructive
pulmonary disease: A comprehensive and critical evaluation. Dis Management Health Outcomes 2003;
11:311-319
954
Foster G, Taylor SJC, Eldridge SE, Ramsay J, Griffiths CJ. Self-management education programmes by
lay leaders for people with chronic conditions. Cochrane Database Syst Rev 2007, Issue 4. Art No:
CD005108
955
Jordan JE, Osborne RH. Chronic disease self-management programs: challenges ahead. Med J Aust
2007; 186:84-87
956
Effing T, Monninkhof EM, van der Valk PDLPM, van der Palen J, van Herwaaden CLA, Partridge MR,
Walters EH, Zielhuis GA. Cochrane Database Syst Rev 2007, Issue 4. Art No: CD002990
957
Turnock AC, Walters EH, Walters JA, Wood-Baker R. Action plans for chronic obstructive pulmonary
disease. Cochrane Database Syst Rev 2005, Issue 4: Art no: CD005074
958
Kessler R, Stahl E, Vogelmeier C, Haughney J, et al. Patient understanding, detection, and experience of
COPD exacerbations. An observational, interview-based study. Chest 2006; 130:133-142
959
McGeoch GRB, Willsman KJ, Dowson CA, Town GI, et al. Self-management plans in the primary care
of patients with chronic obstructive pulmonary disease. Respirology 2006; 11:611-618
116
patient-identified exacerbations, but no significant differences between groups in use of health
care resources960.
Most studies have addressed group education, even with self-management. However, there are
reasons to expect that an individualised approach might be helpful (although resource-intensive).
One randomised trial evaluated the effects of a “dyspnoea self-management program”961, which
gave each patient three hours of individual identification of triggers for dyspnoea, strategies to
control breathlessness, understanding dyspnoea, using medications correctly, and provision of a
personalised reference manual. This extended over four sessions in 8 weeks. In addition regular
exercise was emphasised and each patient received an individualised home exercise program. The
36 patients who completed the program had no changes in Borg Dyspnoea levels with exercise,
non-significant improvement in exercise endurance performance, no significant change in
dyspnoea scales, but small improvements in some sub-scales. Small numbers and no “usual
treatment” control group limited the power to detect true differences. However, comparison with
two other groups was instructive. The first comparison group included patients who undertook
dyspnoea self-management training with exposure to four treadmill walking sessions over the 8week program. The second group undertook a full exercise training program for the 8 weeks. The
latter group did achieve significant improvements in exercise performance, dyspnoea during
exercise, and a number of HRQoL parameters.
In assessing and educating patients to achieve health gains from PR it may be useful to
understand the specific limitations imposed by their lung disease and to help them set goals to
overcome or minimize those limitations. Goal achievement can then be used as an outcome
measure. Two systematic reviews are relevant. In the first, a mix of rehabilitation interventions
was examined962, evaluating randomised controlled trials on the therapeutic effectiveness of goal
setting for patients with disabilities due to degenerative diseases (including COPD). Thirteen
studies that met the criteria of goal-setting within a rehabilitation program were identified. Small
improvements in adherence to treatment recommendations by patients were noted, and larger
improvements in some specific patient performance, but the findings were inconsistent. In the
second, scaled scores of goal achievement in older people undergoing rehabilitation for a variety
of conditions (not including COPD) were evaluated963. Goal attainment scaling had good
reliability, validity and sensitivity, but goal setting had lower reliability and sensitivity.
960
Wood-Baker R, McGlone S, Venn A, Walters EH. Written action plans in chronic obstructive
pulmonary disease increase appropriate treatment for acute exacerbations. Respirology 2006; 11:619-626
961
Stulbarg MS, Carrieri-Kohlman V, Demir-Deviren S, Nguyen HQ, et al. Exercise training improves
outcomes of a dyspnea self-management program. J Cardiopulm Rehabil 2002; 22:105-108
962
Levack WM, Taylor K, Siegert RJ, Dean SG, et al. Is goal planning in rehabilitation effective? A
systematic review. Clin Rehabil 2006; 20:739-755
963
Hurn J, Kneebone I, Cropley M. Goal setting as an outcome measure: A systematic review. Clin Rehabil
2006; 20:756-772
117
EDUCATION IN PULMONARY
REHABILITATION
KEY POINTS
1)
Behavioural modification approaches:
•
help smokers quit smoking
•
improve adherence to medications and to exercise
and diet recommendations
•
increase self-efficacy for shared care
2)
Education should be part of a comprehensive
pulmonary rehabilitation program for people
with chronic lung diseases
Physiotherapy
A range of physical therapies has been applied in COPD, mostly adapted from other conditions.
Secretion clearance
Difficulty with clearance of respiratory secretion is an issue in people with bronchiectasis or
severe chronic bronchitis, especially during exacerbations. Coughing can be ineffective because it
produces flow-limitation, and it can also cause fatigue. Assisted or directed huffing may be a
partial solution, and it has benefit in bronchiectasis964, though no evidence has been provided in
COPD even when there are excessive or tenacious secretions965. Postural drainage, of benefit in
bronchiectasis, also has no published evidence of benefit in COPD. A systematic review of
“bronchial hygiene therapy” identified ten randomised controlled trials including only 153 people
with COPD and bronchiectasis966. Different outcome measures prevented statistical aggregation,
but significant sputum clearance from the lung was shown in the 67 patients who had a positive
result, without demonstrable change in lung function or health status. In patients with cystic
fibrosis directed coughing was additive to postural drainage in clearing secretions967,968, but this
therapy may be associated with significant hypoxaemia969. A recent systematic review of “chest
964
Hietpas BG, Roth RD, Jensen WM. Huff coughing and airway patency. Respir Care 1979; 24:710-713
Kiriloff LH, Owens GR, Rogers RM, Mazzacco MC. Does chest physiotherapy work? Chest 1985;
88:436-444
966
Jones AP, Rowe BH. Bronchopulmonary hygiene physical therapy in chronic obstructive pulmonary
disease and bronchiectasis. The Cochrane Library 1998; Issue 3
967
Sutton PP, Lopez-Vidriero MT, Pavia D. Assessment of percussion, vibratory-shaking and breathing
exercises in chest physiotherapy. Am Rev Respir Dis 1985; 6:147-152
968
Pryor JA, Webber BA, Hodson ME, Baten JC. Evaluation of the forced expiration technique as an
adjunct to postural drainage in the treatment of cystic fibrosis. Br Med J 1979; 2:417-418
969
McDonnell T, McNicholas WT, Fitzgerald MX. Hypoxaemia during chest physiotherapy in patients
with cystic fibrosis. Ir J Med Sci 1986; 155:345-348
965
118
physiotherapy” in cystic fibrosis from 1966 to the present found no randomised or quasirandomised or cross-over trials with a control arm, though short-term uncontrolled cross-over
trials suggested some benefit from sputum clearance techniques970.
Sputum clearance with a simple mechanical device, the Flutter VRP1TM, has been studied in a
small comparison with sham therapy (10 patients with COPD and mucus hypersecretion in each
group) over 3 months. There were small (statistically but not clinically significant) changes in
lung function and 12-minute walk distance (12WD) in the treatment group compared to the sham
treated group, and significant improvement in COPD symptom scores over baseline levels in the
treatment group971. Even for patients with severe COPD (and other respiratory problems requiring
non-invasive ventilation) there are devices being trialled, such a mechanical insufflationexsufflation device. In such people (including nine with chronic respiratory failure due to COPD)
this was well tolerated and effective in clearing troublesome airway secretions972. Other devices
operate on similar principles, but no trials have been found giving significant benefits.
Breathing Retraining Techniques
The goal of breathing retraining techniques (BRT) is to reduce dyspnoea and improve the
mechanical efficiency of ventilation. Dyspnoea has been associated with dyssynchrony of
thoraco-abdominal motion973,974.An early observational study conducted in 22 patients with
severe COPD provided treadmill training for six weeks, adding BRT for 10 of the patients for the
final three weeks while the controls continued treadmill training alone975, and concluded greater
increments in exercise capacity were seen in the BRT group. BRT includes diaphragmatic
breathing (DB)976,977, pursed lips breathing (PLB)978, and teaching thoraco-abdominal
synchrony979. Many patients with severe COPD actually develop these techniques for themselves,
but studies have shown inconsistent results.
In spite of physiologic observations relating to beneficial breathing pattern, and widely applied
recommendation for DB and PLB to reduce breathlessness, there has been essentially no wellpowered randomised controlled trial of any of these therapy techniques in COPD, particularly
970
van der Schans C, Prasad A, Main E. Chest physiotherapy compared to no chest physiotherapy for cystic
fibrosis. Cochrane Database of Systematic Reviews 2001; Issue 4
971
Weiner P, Zamir D, Waizman J, Weiner M. Physiotherapy in chronic obstructive pulmonary disease:
oscillatory breathing with flutter VRP1. Harefuah 1996; 131:14-17
972
Winck JC, Gonçalves MR, Lourenço C, Viana P, et al. Effects of mechanical insufflation-exsufflation
on respiratory parameters for patients with chronic airway secretion encumbrance. Chest 2004; 126:774780
973
Sharp J, Goldberg N, Druz W, et al. Thoraco-abdominal motion in chronic obstructive pulmonary
disease. Am Rev Respir Dis 1977; 115:47-56
974
Delgato H, Braun S, Skatrud B, et al. Chest wall and abdominal motion during exercise in patients with
chronic obstructive pulmonary disease. Am Rev Respir Dis 1982; 126:200-205
975
Casciari RJ, Fairshter RD, Harrison A, et al. Effects of breathing retraining in patients with chronic
obstructive pulmonary disease. Chest 1981;79:393-398
976
Girodo M, Ekstrand KA, Metivier GJ. Deep diaphragmatic breathing: rehabilitation exercises for the
asthmatic patient. Arch Phys Med Rehabil 1992; 73:717-720
977
Gosselink RA, Wagenaar RC, Rijswijk H, et al. Diaphragmatic breathing reduces efficiency of breathing
in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995; 151:1136-1142
978
Tiep BL, Burns M, Kao D, et al. Pursed lips breathing training using ear oximetry. Chest 1986; 90:218221
979
Willeput R, Vashaudez JP, Landers D, Nys A, et al. Thoracoabdominal motion during chest
physiotherapy in patients affected by chronic obstructive lung disease. Respiration 1983; 44:204-214
119
from the viewpoint of dyspnoea or health status980. A review of breathing re-training in
asthmatics identified five randomised controlled trials meeting Cochrane Review criteria, all of
them small. The largest showed reduced use of rescue medications, but no overall conclusions
about the benefit or otherwise of this technique in asthma could be derived981. Since this
systematic review, a well-designed study has shown that encouragement of slower and deeper
breathing patterns during exercise training, using ventilation feedback techniques, provided
greater benefits from endurance training than allowing subjects to use their own breathing
patterns982.
Pursed-lip breathing (PLB)
PLB alters respiratory muscle functions in favour of enhanced efficiency and reduced work of
breathing983. Dyspnoea can be improved with PLB984, and the extent of relief has been associated
with reduced respiratory rate and increased tidal volume985. However, in an observational study,
PLB has been reported to increase air trapping and work of breathing986. PLB was found to have
variable effects in eight COPD patients, but reduction in dynamic hyperinflation was associated
with lower levels of perceived dyspnoea987.
Diaphragmatic breathing (DB)
DB involves encouraging diaphragmatic excursion while reducing upper rib cage motion, which
causes the abdominal wall to move outwards during inhalation. It therefore aims to improve chest
wall motion and the distribution of ventilation to better-perfused lower lung zones. It has been
prescribed for at least 50 years, with some accumulated experimental rationale. Improved
ventilation (with reduced respiratory rate and arterial carbon dioxide levels) has been
demonstrated988,989, although increased dys-synchrony, work of breathing and dyspnoea have also
990,991,992,993
. Recent
been found, without improvement in regional ventilation to lung bases
980
Breslin EH. Breathing retraining in chronic obstructive pulmonary disease. J Cardiopulm Rehabil 1995;
15:25-33
981
Holloway E, Ram FSF. Breathing exercises for asthma. Cochrane Database Syst Rev 2001; Issue 4
982
Collins EG, Langbein WE, Fehr L, et al. Can ventilation-feedback training augment exercise tolerance
in patients with chronic obstructive pulmonary disease? Am J Respir Crit Care Med 2008; 177:844-852
983
Breslin EH. The pattern of respiratory muscle recruitment during pursed-lip breathing. Chest 1992;
101:75-78
984
Ingram RH, Schilder DP. Effect of pursed lips expiration on the pulmonary pressure-flow relationship in
obstructive lung disease. Am Rev Respir Dis 1967; 96:381-388
985
Mueller RE, Petty TL, Filley GF. Ventilation and arterial blood gas changes induced by pursed lips
breathing. J Appl Physiol 1970; 28:784-789
986
Tiep BL, Burns M, Kao D, et al. Pursed lips breathing training using ear oximetry. Chest 1986; 90:218221
987
Spahija J, de Marchie M, Grassino A. Effects of imposed pursed-lips breathing on respiratory mechanics
and dyspnea at rest and during exercise in COPD. Chest 2005; 128:640-650
988
Miller WF. A physiologic evaluation of the effects of diaphragmatic breathing training in patients with
chronic pulmonary emphysema. Am J Med 1954; 17:471-477
989
Sackner MA, Silva G, Banks JM, et al. Distribution of ventilation during diaphragmatic breathing in
obstructive lung disease. Am Rev Respir Dis 1974; 109:331-337
990
Sackner MA, Silva G, Banks JM, et al. Distribution of ventilation during diaphragmatic breathing in
obstructive lung disease. Am Rev Respir Dis 1974; 109:331-337
991
Sackner MA, Gonzalez H, Rodriguez M, Belsito A, et al. Assessment of asynchronous and paradoxic
motion between rib cage and abdomen in normal subjects and in patients with chronic obstructive
pulmonary disease. Am Rev Respir Dis 1984; 130:588-593
992
Vitacca M, Clini E, Bianchi L, Ambrosino N. Acute effects of deep diaphragmatic breathing in COPD
patients with chronic respiratory insufficiency. Eur Respir J 1998; 11:408-415
120
research suggests greater benefits from endurance training can result from deep slow breathing
during training994.
Given the lack of clear benefit in well-conducted trials, and the evidence of adverse effects,
retraining of patients with COPD for PLB and DB cannot be strongly recommended as routine
group exercises. However, in view of some observations of improved dyspnoea in some patients,
it seems sensible to assess individuals for poor breathing technique and direct individual training
where necessary.
Positioning and Relaxation
The lean forward position, with fixation of the shoulder girdle to enhance the action of the
995, 996
. Many patients adopt this
accessory muscles of ventilation, can relieve breathlessness
position themselves without receiving specific training. In addition, relaxation training can help to
avert the panic associated with breathlessness (see also above). Slumped and upright seated
postures have been compared in 14 patients with moderately severe COPD, and no improvements
in cardiovascular or respiratory functions were found997.
Massage and manipulation
These are sometimes recommended in asthma and COPD. A systematic review of randomised
trials of “manual therapy” in asthma998 found five randomised controlled trials amounting to 290
patients. One trial of chiropractic manipulation was methodologically well done, but it and only
one other trial of the same therapy showed significant differences between this therapy and a
sham procedure. Otherwise trials were inadequate to show statistical differences with “chest
physiotherapy”, “footzone therapy”, “massage therapy” or “relaxation” in asthma.
Task Optimisation
Task simplification may appear counter-intuitive when the therapeutic goal is physiological
training, but task performance can be optimised without sacrificing true training. After all, the
aim of PR is to “achieve and maintain the individual’s maximum level of independence and
functioning in the community”999. Total daily energy expenditure is often increased in patients
with COPD1000, perhaps in part due to raised resting energy expenditure1001, and in part due to
993
Gosselink RA, Wagenaar RC, Rijswijk H, et al. Diaphragmatic breathing reduces efficiency of breathing
in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995; 151:1136-1142
994
Collins EG, Langbein WE, Fehr L, et al. Can ventilation-feedback training augment exercise tolerance
in patients with chronic obstructive pulmonary disease? Am J Respir Crit Care Med 2008; 177:844-852
995
Barach AL. Chronic obstructive pulmonary disease: postural relief of dyspnoea. Arch Phys Med Rehabil
1974; 55:494-504
996
Sharp JT, Druz WS, Moisan T, et al. Postural relief of dyspnoea in severe chronic obstructive
pulmonary disease. Am Rev Respir Dis 1980; 122:201-211
997
Landers MR, McWhorter JW, Filibeck D, Robinson C. Does sitting posture in chronic obstructive
pulmonary disease really matter? J Cardiopulm Rehabil 2006; 26:405-409
998
Hondras MA, Linde K, Jones AP. Manual therapy for asthma. Cochrane Database of Syst Rev 2001;
Issue 4
999
Fishman AP. NIH Workshop summary. Pulmonary rehabilitation research. Am J Respir Crit Care Med
1994; 149:825-833
1000
Baarends EM, Schols AM, Pannemans DL, et al. Total free living energy expenditure in patients with
severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1997; 155:549-554
1001
Creutzberg EC, Schols AMWJ, Bothmer-Quaedvlieg FCM, Wouters EFM. Prevalence of an elevated
resting energy expenditure in patients with chronic obstructive pulmonary disease in relation to body
composition and lung function. Eur J Clin Nutr 1998; 52:396-401
121
mechanical inefficiency of human movement, of breathing or of specific muscle groups1002.
Training in activities of daily living (ADL) not only includes the overall exercise training but
learning how to work efficiently and therefore minimise the daily metabolic costs associated with
ADLs, allowing more energy for recreational and social activities. Pacing, and breathing
techniques linking effort to the respiratory cycle during ADLs, avoiding anxiety-provoking
situations, mastery training, and cognitive behaviour therapy all contribute to energy
optimisation. Further, recent research has shown that COPD patients have significant difficulties
with coordination, balance and mobility (correlated with the severity of FEV1 impairment and not
the level of hypoxaemia), which may compound strength, endurance and behavioural
problems1003. While it is not possible to design a randomised controlled trial to prove the benefits
1004,1005,1006
.
of energy conservation, it is logical, and an intrinsic part of PR programs worldwide
PHYSIOTHERAPY
KEY POINTS
1)
Secretion clearance techniques are useful where there are
tenacious or increased secretions
2)
Breathing re-training may reduce dyspnoea
3)
Pursed-lip breathing can reduce dyspnoea
4)
Slow deep breathing during training may increment benefits of
exercise training
5)
Gait and mobility assessment help to individualise training
6)
Water-based exercise is of unproven benefit in COPD
7)
Massage and manipulation are of unproven benefit in COPD
1002
Baarends EM, Schols AM, Akkermans MA, Wouters EF. Decreased mechanical efficiency in clinically
stable patients. Thorax 1997; 52:981-986
1003
Butcher SJ, Meshke JM, Sheppard MS. Reductions in functional balance, coordination, and mobility
measures among patients with stable chronic obstructive pulmonary disease. J Cardiopulm Rehabil 2004;
24:274-280
1004
Ries AL. Position paper of the American Association of Cardiovascular and Pulmonary Rehabilitation:
Scientific basis of pulmonary rehabilitation. J Cardiopulm Rehabil 1990; 10:418-441
1005
Celli BR, Snider GL, Heffner J, Tiep B, Ziment I, et al. Standards for the diagnosis and care of patients
with COPD. Am J Respir Crit Care Med 1995; 152 (Suppl 5):S78-S121
1006
Rashbaum I, Whyte N. Occupational therapy in pulmonary rehabilitation: Energy conservation and
work simplification techniques. Phys Med Rehabil Clin N Am 1996; 7:325-340
122
Psychological Interventions
Prevalence and Impact
There is controversy about the importance of psychological impairments and their treatment in
chronic lung disease. American guidelines for PR formerly stated that “depression and anxiety
may affect a substantial number of patients with COPD, but [they] are not necessarily
concomitants of chronic lung disease.”1007 On the other hand, recently updated guidelines of
American and European professional societies1008 state “Chronic respiratory disease is associated
with increased risk for anxiety, depression, and other mental health disorders”, indicating a
significant shift in understanding. Furthermore, they acknowledge the significant impact on other
aspects of the experience of people with COPD – “psychological distress ..[in].. COPD predicts
impaired quality of life and restricted ADLs. Functional capacity is more strongly associated with
emotional/psychosocial factors…than with traditional physiological indicators.”1009
It is true that there are inconsistencies among studies of psychological issues, and many of them
have been poorly controlled. In a systematic review1010, rates of depression were generally not
significantly higher than in matched populations – between 7% and 42%. A number of robust
though non-controlled studies, however, were not included, and anxiety was not addressed. A
cross-sectional study of 109 oxygen-dependent patients with severe COPD showed 57% had
significant depressive symptoms, and 18% were severely clinically depressed1011. Other crosssectional studies in non-selected populations have confirmed that depression is not uncommon in
stable patients with severe COPD1012,1013. Observed risks of depression were 2.5-fold higher in
people with severe COPD than in age-matched controls1014, and this finding is especially so in
smokers. Fear and anxiety are expected to be associated with episodes of dyspnoea1015, and in turn
these disorders can add to the awareness of uncomfortable breathing. The prevalence of clinically
significant anxiety also varies widely – between 10% and 96%1016.Mental health issues predict
worse HRQOL and restrictions in activities of daily living1017, but appear not to be associated
with worse survival in COPD.
1007
AACVPR/ACCP Pulmonary Rehabilitation Guidelines Panel. Pulmonary Rehabilitation. Joint
AACVPR/ACCP evidence-based guidelines. Chest 1997; 112:1363-1396
1008
Nici L, Donner C, Wouters E, Zuwallack R, Ambrosino N, et al. American Thoracic Society/European
Respiratory Society Statement on Pulmonary Rehabilitation. Am J Respir Crit Care Med 2006; 173:13901413
1009
Ries AL, Bauldoff GS, Carlin BW, Casaburi R, et al. Pulmonary Rehabilitation: Joint ACCP/AACVPR
Evidence-Based Clinical Practice Guidelines. Chest 2007; 131:4-42
1010
van Ede L, Yzermans CJ, Brouwer HJ. Prevalence of depression in patients with chronic obstructive
pulmonary disease: A systematic review. Thorax 1999; 54:688-692
1011
Lacasse Y, Rousseau L, Maltais F. Prevalence of depressive symptoms and depression in patients with
severe oxygen-dependent chronic obstructive pulmonary disease. J Cardiopulm Rehabil 2001; 21:80-86
1012
Kostianev S, Mitrev I, Hodgev V, et al. Dyspnoea, depression and anxiety in patients with chronic
obstructive pulmonary disease. Bulg Med J 2001; 9:23-25
1013
Yohannes AM, Roomi J, Baldwin RC, Connolly MJ. Depression in elderly outpatients with disabling
chronic obstructive pulmonary disease. Age & Ageing 1998; 27:155-160
1014
van Manen JG, Bindels PJ, Ilzermans CJ, et al. Prevalence of comorbidity in patients with chronic
airways obstruction and controls over the age of 40. J Clin Epidemiol 2001; 54:287-293
1015
Heim E, Blaser A, Waidelich E. Dyspnea: psychophysiologic relationships. Psychosom Med 1972;
34:405-423
1016
Hynninen KM, Breitve MH, Wiborg AB, et al. Psychological characteristics of patients with chronic
obstructive pulmonary disease: a review. J Psychosom Res 2005; 59:429-443
1017
Yohannes AM, Roomi J, Waters K, et al. Quality of life in elderly patients with COPD: measurement
and predictive factors. Respir Med 1998; 92:1231-1236
123
Despite methodological inconsistencies, the research does indicate that, as in other chronic
diseases, psychological impairment presents significant challenges with respect to effective
treatment of COPD. Health related quality of life (HRQoL) impairment in people with COPD is
reflected by reduced energy, mobility and sleep, poor emotional function such as depression,
anxiety and dissatisfaction with life, and somatic preoccupation1018. Poor emotional functioning
has been found a univariate predictor of increased mortality, increased health-care utilisation,
decreased medication compliance and reduced productivity1019. A useful review has recently been
published addressing prevalence, risks, diagnostic issues and treatments for anxiety and
depression in late-stage COPD1020.
Depression
Estimates of depression in patients with COPD vary from 6% to 60%1021,1022. Such a wide range
can be explained, at least in part, by differences in research methodologies and in characteristics
of the study populations including severity of COPD1023 However, it is generally accepted that the
prevalence rate is around 40%1024. Depression is associated with increased morbidity and
mortality1025 in COPD patients. It impacts upon a range of health outcomes including poorer
physical and social functioning, an increased symptom burden and rates of hospitalization and
contributes to the failure to quit smoking or maintain abstinence1026 A small number of studies
have attempted to find a correlation between disease severity and depressive symptomatology in
patients with COPD. One study found that patients with severe COPD had a 2.5 times greater risk
of depression than controls and this was increased in patients with more severe physical
limitation1027.
Anxiety
As with depression the literature is unclear on the prevalence rates of anxiety in patients with
COPD. An analysis by Brenes found that studies reported rates between 10% and 49%1028 A
1018
Crockett AJ, Cranston JM, Moss JR, et al. The impact of anxiety, depression and living alone in
chronic obstructive pulmonary disease. Qual Life Res 2002; 11:309-316
1019
Katon W, Von Koroff M, Lin E, et al. Distressed High Utilizers of Medical Care DSM–111-R
Diagnoses and Treatment Needs. Gen Hosp Psych 1990; 12:355-362
1020
Hill K, Geist R, Goldstein RS, Lacasse Y. Anxiety and depression in and-stage COPD. Eur Respir J
2008; 31:667-677
1021
Van Ede L, Yzermans CJ, Brouwer HJ. Prevalence of depression in patients with chronic obstructive
pulmonary disease: A systematic review. Thorax 1999; 54:688-692.
1022
Norwood R. Prevalence and impact of depression in chronic obstructive pulmonary disease patients.
Curr Opin Pul Med 2006;12:113-117
1023
Mikkelsen RL, Middelboe T, Pisinger C. Anxiety and depression in patients with chronic obstructive
pulmonary disease (COPD). A Review. Nord J Psychiatry 2004;58(1):65-70
1024
Yohannes AM, Baldwin RC, Connolly MJ. Prevalence of sub-threshold depression in elderly patients
with chronic obstructive pulmonary disease. Internal J Geriatric Psychiatr 2003;18:412-416
1025
Yohannes AM, Baldwin RC, Connolly MJ. Predictors of 1-year mortality in patients discharged from
hospital following acute exacerbation of chronic obstructive pulmonary disease. Age Ageing 2005;34:491496
1026
Ng TP, Niti M, Tan WC et al. Depressive symptoms and chronic obstructive pulmonary disease: effect
on mortality, hospital readmission, symptom burden, functional status, and quality of life. Arch Intern Med
2007;167:60-67
1027
Van Manen JG, Bindels PJ, Dekker FW, et al. Risk of depression in patients with chronic obstructive
pulmonary disease and its determinants. Thorax 2002;57:412-416
1028
Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact and treatment.
Psychosom Med 2003;65:963–970
124
meta-analysis estimated rates at approximately 36%1029. Research on the different subtypes of
anxiety disorders in COPD patients is limited. Studies have estimated of rates of Generalised
Anxiety Disorder (GAD) between 10% and 33% and Panic Disorder rates between 8% and
67%1030,1031,1032,1033,,which are much higher than rates in the general and healthy elderly
population1034, and in patients with other chronic medical conditions1035,1036,1037.
Coexisting depression and anxiety
These comorbidities occur together commonly in COPD patients, with prevalence rates estimated
to be between 23% and 64%1038,1039,1040,1041,1042,1043, with increased rates even in people with mild
COPD1044, and higher rates in women than men1045,1046. This combination has been linked to
higher levels of symptoms, worse quality of life, impaired functional status and re-presentation
after emergency treatment in COPD patients1047,1048,1049. Depression and anxiety are under1029
Rose C, Wallace L, Dickson R, et al. The most effective psychologically-based treatments to reduce
anxiety and panic in patients with chronic obstructive pulmonary disease (COPD): a systematic review.
Patient Educ Couns 2002;47:311-318
1030
Porzelius J, Vest M, Nochomovitz M. Respiratory function, cognitions, and panic in chronic obstructive
pulmonary patients. Behav Res Ther 1992;30:75–77
1031
Moore M, Zebb B. The catastrophic misinterpretation of psychological distress. Behav Res Ther 1999;
37:1105-1118
1032
Pollack MH, Kradin KR, Otto MW, et al. Prevalence of panic in patients referred for pulmonary
function testing at a major medical center. Am J Psychiatry 1996;153:110-113
1033
Dowson CA, Kuijer RG, Mulder RT. Anxiety and self-management behaviour in chronic obstructive
pulmonary disease: what has been learned? Chron Respir Dis. 2004;1:213-220
1034
Krasucki C, Howard R, Mann A. The relationship between anxiety disorders and age. Int J Geriatr
Psychiatry 1998;13:79-99
1035
Kvaal K, Macijauskiene J, Engedal K, et al. High prevalence of anxiety symptoms in hospitalized
geriatric patients. Int J Geriatr Psychiatry 2001;16:690-693
1036
Hansen M, Fink P, FrydenbergM, et al. Mental disorders among internal medical inpatients: prevalence,
detection and treatment status. J Psychosom Res 2001;50:199-204
1037
Herrmann C. International experiences with the Hospital Anxiety and Depression Scale – a review of
validation data and clinical results. J Psychosom Res 1997;42:17–41
1038
Cleland JA, Lee AJ, Hall S. Associations of depression and anxiety with gender, age, health-related
quality of life and symptoms in primary care COPD patients. Fam Prac 2007;24:217-223
1039
Kim HF, Kunik ME, Molinari VA, et al. Functional impairment in COPD patients: the impact of
anxiety and depression. Psychosomatics 2000;41:465-471
1040
Yohannes AM, Baldwin RC, Connolly MJ. Depression and anxiety in elderly outpatients with chronic
obstructive pulmonary disease: prevalence, and validation of the BASDEC screening questionnaire. Int J
Geriatr Psychiatry 2000;15:1090-1096
1041
Kunik ME, Roundy K, Veazey C. Surprisingly high prevalence of anxiety and depression in chronic
breathing disorder. Chest 2005;127:1205-1211
1042
Ferguson CJ, Stanley M, Souchek J, et al. The utility of somatic symptoms as indicators of depression
and anxiety in military veterans with chronic obstructive pulmonary disease. Depress Anxiety 2006;23:4249
1043
Mikkelsen RL, Middelboe T, Pisinger C, et al. Anxiety and depression in patients with chronic
obstructive pulmonary disease (COPD). A review. Nord J Psychiatry 2004;58:65-70
1044
Di Marco F, Verga M, Reggente M, et al. Anxiety and depression in COPD patients: The roles of
gender and disease severity. Respir Med 2006;100:1767-1774
1045
Chavannes NH, Huibers MJH, Schermer TRJ, et al. Associations of depressive symptoms with gender,
body mass index and dyspnea in primary care COPD patients. Fam Pract 2005;22:604-607
1046
Laurin C, Lavoie KL, Bacon SL, et al. Sex differences in the prevalence of psychiatric disorders and
psychological distress in patients with chronic obstructive pulmonary disease. Chest 2007;132:148-155
1047
Cully JA, Graham DP, Stanley MA, et al. Quality of life in patients with chronic obstructive pulmonary
disease and comorbid anxiety and depression. Psychosomatics 2006;47:312-319
125
diagnosed and hence under-treated in patients with COPD1050, perhaps because of confusion
between the somatic symptoms (especially dyspnoea) related to pathophysiology and true mental
health disorder1051,1052.
Given the impact of psychological impairment on COPD patients and their carers, and the
expected increase of the disease burden as the population ages (especially among women)1053,
there is a need to address methodological issues in research on all COPD populations.
One problem with estimating prevalence of mood disorders in people with COPD (and their
carers) is the variety of measurement tools. These vary from broad-based psychological health
questionnaires to specific anxiety or depression inventories and structured interviews for a
codable psychiatric diagnosis. As with most chronic health problems, patients with COPD
experience many negative psychological effects that impact on their quality of life. Whether the
underlying disease is responsible, or the impact is greater in those with poor mental health
resources is difficult to determine. In a longitudinal study of people with chronic respiratory and
cardiac diseases and those with chronic back pain, 1784 people were followed for 6 years,
significant predictors of deterioration in physical functioning were low income, excess alcohol
consumption, external locus of control and other social determinants, suggesting underlying
disease is a less important risk factor for changes in physical functioning1054.
Interventions for mental health disorders in COPD
Pharmacological Therapy
Studies evaluating drug therapy for COPD patients with depression and anxiety are inconclusive.
Early studies did not demonstrate improvement in depression or anxiety from antidepressant
treatment in patients with COPD1055,1056. Later relatively small trials (RCTs and case series) have
shown patients with end-stage COPD might benefit from treatment with Selective Serotonin
Reuptake Inhibitors (SSRIs) or Tricyclic Antidepressants (TCAs) when significant depressive or
anxiety symptoms are present1057,1058,1059,1060. It is important to be aware, however, that
1048
Kim HF, Kunk ME, Molinari VA, et al. Functional impairment in COPD patients: the impact of anxiety
and depression. Psychosomatics 2000;41:465-471
1049
DahlГ©n I, Janson MD. Anxiety and depression are related to the outcome of emergency treatment in
patients with obstructive pulmonary disease. Chest 2002;122:1633-1637
1050
Kunik ME, Roundy K, Veazey C. Surprisingly high prevalence of anxiety and depression in chronic
breathing disorder. Chest 2005;127:1205-1211
1051
Yohannes AM, Baldwin RC, Connolly MJ. Depression and anxiety in elderly patients with chronic
obstructive pulmonary disease. Age Ageing 2006;35:457-479
1052
Simon NM, Weiss AM, Kradin R, et al. The relationship of anxiety disorders, anxiety sensitivity and
pulmonary dysfunction with dyspnea-related distress and avoidance. J Nerv Ment Dis 2006;194:951-957
1053
Lopez, AD, Shibuya K, Rao C, Mathers CD, et al. Chronic obstructive pulmonary disease: current
burden and future projections. Eur Respir J 2006; 27:397-412
1054
Mackenbach JP, Borsboom GJ, Nusselder WJ, et al. Determinants of levels and changes of physical
functioning in chronically ill persons: results from the GLOBE Study. J Epidemiol Community Health
2001; 55:631-638
1055
Light RW, Merrill EJ, Despars J, et al. Doxepin treatment of depressed patients with chronic obstructive
pulmonary disease. Arch Intern Med 1986;146:1377-1380
1056
Gordon GH, Michaels TM, Mahutte CK, et al. Effect of desipramine on control of ventilation and
depression scores in patients with severe chronic obstructive pulmonary disease. Psychiatry Res
1985;15:25-32
1057
Lacasse Y, Beaudoin L, Rousseau L, et al. Randomized trial of paroxetine in end-stage COPD. Mondali
Arch Chest Dis 2004;61:140-147
126
antidepressants with sedating properties, such as the TCAs and mirtazipine, may increase the risk
of respiratory depression in patients with moderate-severe COPD, while SSRIs combined with
anxiolytics have a relatively small potential for pulmonary side effects and may be effective for
coexisting depression and anxiety1061. Anxiolytics (especially benzodiazepines) are best avoided
because of their potential for dependence, drug interactions and side effects1062, such as accident
proneness, a problem of particular concern for people using domiciliary oxygen therapy, where
equipment and oxygen tubing increase the risk of injury. Buspirone, a non-benzodiazepine, has
been studied in two RCTs, with diverging effects being reported for anxiety, dyspnoea and
adverse effects1063,1064.
Psychological Treatments
There is a paucity of research on psychological treatments for anxiety and depression in patients
with COPD. A systematic review concluded there was insufficient evidence to recommend (or
withhold) psychological based interventions to reduce anxiety in COPD although methodological
problems limit further conclusions1065. A small number of clinical studies have assessed the
efficacy of Cognitive Behaviour Therapy (CBT) on depression and anxiety in COPD
patients1066. Significant improvements in anxiety and depression scores in an elderly population
of COPD patients have been shown from the implementation of a single 2-hour session of CBT
compared with education alone1067. Upon completion of a CBT self-help education programme,
participants demonstrated less irrational reasoning and psychosocial disability although no
reduction in anxiety symptoms1068. In another study, six sessions of CBT produced a sustained
improvement in exercise tolerance in people with moderately severe COPD, without any changes
1058
Borson S, McDonald GJ, Gayle T, et al. Improvement in mood, physical symptoms, and function with
nortriptyline for depression in patients with chronic obstructive pulmonary disease. Psychosomatics
1992;33:190–201
1059
Smoller JW, Pollack MH, Systrom D, et al. Sertraline effects on dyspnea in patients with obstructive
airways disease. Psychosomatics 1998;39:24-29
1060
Silvertooth EJ, Doraiswamy PM, Clary GL, et al. Citalopram and quality of life in lung transplant
recipients. Psychosomatics 2004; 45:271-272
1061
Smoller JW, Pollack MH, Rosenbaum JF, et al. Panic anxiety, dyspnea, and respiratory disease.
Theoretical and clinical considerations. Am J Respir Crit Care Med 1996;154:6-17
1062
Furukawa TA, Streiner DL, Young LTl. Antidepressant and benzodiazepine for major depression.
Cochrane Database Syst Rev 2002, Issue 1: Art no: CD001026
1063
Argyropoulou P, Patakas D, Koukou A, Vasiliadis P, Georgopoulos D. Buspirone effect on anxiety
levels and exercise tolerance in patients with chronic obstructive pulmonary disease. Respiration 1993;
60:216-220
1064
Singh NP, Despars JA, Stansbury DW, Avalos K, Light RW. Effects of buspirone on anxiety levels and
exercise tolerance in patients with chronic airflow obstruction and mild anxiety. Chest 1993; 103:800-804
1065
Rose C, Wallace L, Dickson R. et al. The most effective psychologically-based treatments to reduce
anxiety and panic in patients with chronic obstructive pulmonary disease (COPD): a systematic review.
Patient Educ Couns 2005;47:311-318
1066
Eiser N, West C, Evans S, et al. Effects of psychotherapy in moderately severe COPD: a pilot study.
Eur Respir J 1997;10:1581-1584
1067
Kunik ME, Braun U, Stanley MA, et al. One session cognitive behavioural therapy for elderly patients
with chronic obstructive pulmonary disease. Psychol Med 2001;31:717-723
1068
Lisansky DP, Clough DH. A cognitive-behavioral self-help educational program for patients with
COPD: A pilot study. Psychother Psychosom 1996;65:97–101
127
in anxiety scores1069. A recent systematic review concluded that there is scope for a randomized
trial to evaluate the effectiveness and acceptability of CBT in this medical population1070.
There is no identifiable research published evaluating the effectiveness of Interpersonal
Therapy (IPT) in COPD patients. There is a single study evaluating Supportive Therapy (ST)
for patients who have severe COPD requiring domiciliary oxygen therapy; the nonpharmacologic component was a patient support group. In this study ST enabled these patients to
participate in support groups, entertainment, lectures and other social activities while reducing the
impact of the disease and improving their quality of life1071. Relaxation Therapy (RT) for
patients with COPD has been shown to decrease anxiety and increase HRQOL1072,1073. A metaanalysis found statistically significant beneficial effects on both dyspnea and psychological well
being from the use of RT1074. Other studies have found that Progressive Muscle Relaxation
(PMR) reduces anxiety and decreases dyspnea and airways obstruction1075,1076,1077 and guided
imagery can produce improvements in breathing1078,1079.
HOME CARE
This has long been practised in US centres, albeit with little objective evidence of benefit to
health status or cost savings in observational studies. Home care could be used for a range of
purposes, from home oxygen monitoring to management of exacerbations of COPD. Moreover, a
variety of challenges, funding systems and administrations between different countries make
generalisable recommendations difficult. A systematic review found no consistent evidence of
cost savings or benefits from home care, mainly due to the range of interventions covered1080.
This has been updated recently, with firmer conclusions based on some of the studies detailed
below1081. Improved health related quality of life has been described in Canada1082, though other
earlier studies found fewer benefits and no savings of mortality or conventional
1069
Eiser N, West C, Evans S, et al. Effects of psychotherapy in moderately severe COPD: a pilot study.
Eur Respir J 1997;10:1581-1584
1070
Coventry PA, Gellatly JL. Improving outcomes for COPD patients with mild-to-moderate anxiety and
depression: A systematic review of cognitive behavioural therapy. Br J Health Psychol 2007 April 18;
[Epub ahead of print]
1071
Petty TL. Supportive therapy in COPD. Chest 1998;113:256S-262S
1072
Narsavage GL. Promoting function in clients with chronic lung disease by increasing their perception of
control. Holist Nurs Pract 1997;12:17-26
1073
Broussard R. Using relaxation for COPD. Am J Nurs 1979;11:1962-1963
1074
Devine EC, Pearcy J. Meta-analysis of the effects of psychoeducational care in adults with chronic
obstructive pulmonary disease. Patient Educ Couns 1996;29:167-178
1075
Renfroe KL. Effect of progressive relaxation on dyspnea and state anxiety in patients with chronic
obstructive pulmonary disease. Heart Lung 1988;17:408-413
1076
Acosta F. Biofeedback and progressive relaxation in weaning the anxious patient from the ventilator: a
brief report. Heart Lung 1988;17:299-301
1077
Rosser RM, Denford J, Heslop A. Breathlessness and psychiatric morbidity in chronic bronchitis and
emphysema: a study of psychotherapeutic management. Psychol Med 1983;13:93– 110
1078
Louie SW. The effects of guided imagery relaxation in people with COPD. Occup Ther Int
2004;11:145-159
1079
Moody LE, Fraser M, Yarandi H. Effects of guided imagery in patients with chronic bronchitis and
emphysema. Clin Nurs Res 1993;2:478–486
1080
Shepperd S. Hospital at home versus in-patient hospital care. Cochrane Database Syst Rev 2001; Issue
3
1081
Shepperd S, Iliffe S. Hospital at home versus in-patient hospital care. Cochrane Database Syst Rev
2005; Issue 3
1082
Borbeau J, Julien M, Maltais F, et al. Reduction of hospital utilization in patients with chronic
obstructive pulmonary disease. Arch Intern Med 2003; 163:585-591
128
costs1083,1084,1085,1086. A Spanish trial of 222 COPD patients randomised to usual hospital care or
�home hospitalisation’ from the Emergency Department (ED) found better outcomes (fewer ED
re-visits, better quality of life, better self-management and satisfaction) at lower cost1087. Another
non-randomised analysis of Spanish patients agreeing to supported discharge after initial
stabilisation of an exacerbation showed shorter length of stay without increase in readmission
rates, and with concomitant cost savings1088. In Italy, home care programs for home oxygen
therapy and home mechanical ventilation were evaluated in 34 COPD patients, with a historical
comparison group, and fewer hospital admissions were seen in the home care group1089,1090.
Two randomised controlled trials of early supported discharge of patients from hospital in
exacerbations of COPD were published in 2000. The first showed no disadvantage for the
patients, no difference in subsequent re-hospitalisation, but no indication of the costs of providing
a home support service1091. The second bore the same conclusions, but it also suggested no extra
costs were incurred1092.
Clarification of personal and societal benefits and costs of home care in Australia for patients
with chronic respiratory disease is still required. Smith1093 conducted a randomised study of
patients discharged from hospital following exacerbation of COPD or referred from their GP or
outpatient department, with 48 control patients and 48 patients randomised to a home based
nursing intervention. No significant differences between the two groups could be identified in
terms of QOL, carer wellbeing, or hospital services utilisation over the 12 months of observation,
though there was inadequate follow-up of controls. Davies1094 reported results of a study of
patients with exacerbations of COPD randomised to hospitalisation (n=50) or home care (n=100).
Only 9% of home care patients required subsequent hospital admission, demonstrating that such
an approach is feasible. No differences were seen between the two groups at 3 months in
1083
Bergner M, Hudson LD, Conrad DA, et al. The cost and efficacy of home care for patients with chronic
lung disease. Med Care 1988; 26:566-579
1084
Smith BJ, Appleton SL, Bennett PW, et al. The effect of a respiratory home nurse intervention in
patients with chronic obstructive pulmonary disease (COPD). Aust NZ J Med 1999; 29:718-725
1085
Stewart S, Pearson S, Luke CG, Horowitz JD. Effects of home-based intervention on unplanned
readmissions and out-of-hospital deaths. J Am Geriatr Soc 1998; 46:174-180
1086
Hughes SL, Weaver FM, Giobbie-Hurder A, et al. Effectiveness of team-managed home-based primary
care: a randomised multicenter trial. JAMA 2000; 284:2877-2885
1087
Hernandez C, Casa A, Escarrabill J, et al. Home hospitalsation of exacerbated chronic obstructive
pulmonary disease patients. Eur Respir J 2003; 21:58-67
1088
Sala E, Alegre L, Carrera M, et al. Supported discharge shortens hospital stay in patients hospitalised
because of an exacerbation of COPD. Eur Resppir J 2001; 17:1138-1142
1089
Clini E, Vitacca M, Foglio K, et al. Long-term home care programmes may reduce hospital admissions
in COPD with chronic hypercapnia. Eur Respir J 1996; 9:1605-1610
1090
Haggerty MD, Stockdale-Wooley R, Sreedhar N. Respi-Care: an innovative home care program for the
patient with chronic obstructive pulmonary disease. Chest 1991; 100:607-612
1091
Cotton MM, Bucknall CE, Dagg KD, Johnson MK, et al. Early discharge for patients with
exacerbations of chronic obstructive pulmonary disease: a randomised controlled trial. Thorax 2000;
55:902-906
1092
Skwarska E, Cohen G, Skwarski KM, Lamb C, et al. Randomised controlled trial of supported
discharge in patients with exacerbations of chronic obstructive pulmonary disease. Thorax 2000; 55:907912
1093
Smith BJ, Appleton SL, Bennett PW, Roberts GC, et al. The effect of a respiratory home nurse
intervention in patients with chronic obstructive pulmonary disease. Aust NZ J Med 1999; 29:718-725
1094
Davies L, Wilkinson M, Bonner S, et al. "Hospital at home" versus hospital care in patients with
exacerbations of chronic obstructive pulmonary disease: prospective randomised controlled trial. Brit Med
J 2000; 321:1265-1268
129
hospitalisations, lung function or HRQoL. No economic analysis was reported. Cost savings of
around 50% were identified in a New South Wales randomised controlled trial of home care for a
range of acute medical conditions1095. A nurse-led hotline providing telephone advice on demand
24 hours a day proved safe (no adverse events), and reduced hospital presentations.1096
While it may be feasible to set up hospital outreach or community-based programs to treat sick
patients at home, the studies so far reported have not demonstrated convincingly either efficacy in
COPD or cost-effectiveness. Home-based pulmonary rehabilitation is also a feasible option.
PSYCHOLOGICAL INTERVENTIONS
KEY POINTS
1)
Depression and anxiety are common in COPD
2)
Carers are also affected by psychological stresses
3)
Specific psychological support can reduce anxiety and
panic in breathless patients and their carers
4)
Home care is attractive but of unproven costeffectiveness
Nutritional Interventions
Poor nutritional status is common in severe COPD1097, and is a bad prognostic sign. Body mass
index (BMI) is an independent predictor of mortality in severe COPD1098, and fat free mass
(FFM), which more closely reflects muscle mass, also predicts survival in COPD patients with
normal BMI1099. Loss of lean body mass (FFM) is related to impaired muscle function.
Nutritional Screening Measures
There are many factors proposed to be playing potential roles in nutritional depletion in such
patients, including hypermetabolism in the resting state1100 and insufficient energy intake. Energy
1095
Board N, Brennan N, Caplan GA. A randomised controlled trial of the costs of hospital as compared
with hospital in the home for acute medical patients. Aust NZ J Publ Health 2000; 24:305-311
1096
Roberts MM, Leeder SR, Robinson TD. Nurse-led 24-h hotline for patients with chronic obstructive
pulmonary disease reduced hospital;use and is safe. Inern Med J 2008;
1097
Schols AM. Nutrition in chronic obstructive pulmonary disease. Curr Opin Pulm Med 2000; 6:110-115
1098
Landbo C, Prescott E, Lange P, et al. Prognostic value of nutritional status in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 1999; 160:1856-1861
1099
Vestbo J, Prescott E, Almdal T, Dahl M, et al. Body mass, fat-free body mass, and prognosis in patients
with chronic obstructive pulmonary disease from a random population sample. Findings from the
Copenhagen City Study. Am J Respir Crit Care Med 2006; 173:79-83
1100
Schols AMWJ, Fredrix EWHM, Soeters PB, et al. Resting energy expenditure in patients with chronic
obstructive pulmonary disease. Am J Clin Nutr 1991; 54:983-987
130
expenditure might be consumed in the metabolic demands of the ventilatory muscles, by
inflammation, by smoking, through pharmacotherapeutic or hormonal thermogenesis, or
thermogenesis in digestion or activities. The lead candidates as causes of increased energy
expenditure are the high oxygen cost of breathing in severe COPD (though this is probably not so
at rest), and release of inflammatory mediators, such as TNF-О±, C-reactive protein, etc. Smoking
20 cigarettes a day can also increase energy expenditure by around 10%. Energy intake may be
insufficient for the metabolic demands present in COPD. Depression, abdominal bloating and loss
of appetite, dyspnoea that interferes with chewing and swallowing, inflammatory mediators (see
above), leptins (increased by smoking or inflammation), and inadequate tissue oxygen supply for
muscle (and gut) metabolic activity are all possible causes. The cause of nutritional insufficiency
is probably multi-factorial1101, and systemic inflammation is currently favoured as a major
contributor1102.
Poor nutritional balance may contribute to development or progress of COPD. Predominating
recent research has been the importance of oxidant-antioxidant balance (discussed in 5.2 above),
and a protective effect of fish oils and/or fruit and vegetables as sources of polyunsaturated fatty
acids and antioxidants has been supported by some epidemiological studies1103. Nutritional
advice may have a primary prevention role for COPD and other respiratory conditions, though
evidence directly supporting this is not available.
Nutritional depletion has important consequences for the muscles involved in both ventilation and
locomotion (see above), and there is logic in preventing this depletion, detecting a trend to
depletion early, and to provide nutritional interventions. Initial assessment of patients should
screen for nutritional impairment. Simple advice and more formal education both have roles in
PR. Dietary supplementation was found in a meta-analysis to have been poorly studied (total
patient numbers in the six RCTs, only two of which were double-blind was 277), but supplements
were considered not to have significantly greater benefit than dietary advice1104. Behaviour
change to encourage and entrench better dietary intake is an important role for nutritionists in
COPD.
Anabolic agents have been evaluated in both chronic disease and acute events, in non-respiratory
and respiratory conditions. Ina randomised placebo-controlled trial of 217 COPD patients
nutritional intervention was compared to the same intervention plus nandrolone decanoate, and
greater changes in FFM and ventilatory muscle strength were seen in the depleted patients who
received the anabolic steroid1105. In a longer-term (6-month) randomised placebo-controlled trial
of stanozolol in 23 male COPD patients with nutritional depletion and ventilatory muscle
weakness, preceded by a single testosterone injection, accompanied by IMT and cycle ergometer
1101
Hugli O, Fitting JW. Alterations in metabolism and body composition in chronic respiratory diseases.
Eur Respir Mono 2003; 24:11-22
1102
Agusti AGN, Noguera A, Sauleda J, Busquets X. Systemic inflammation in chronic respiratory disease.
Eur Respir Mono 2003; 24:46-55
1103
Tabak C, Arts IC, Smit HA, et al. Chronic obstructive pulmonary disease and intake of catechins,
flavonols, and flavones: the MORGEN Study. Am J Respir Crit Care Med 2001; 164:61-64
1104
Ferreira IM, Brooks D, Lacasse Y, Goldstein RS. Nutritional support for individuals with COPD: a
meta-analysis. Chest 2000; 117:672-678
1105
Schols AMWJ, Soeters PB, Mostert R, et al. Physiologic effects of nutritional support and anabolic
steroids in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1995;
152:1268-1274
131
training, but no nutritional supplementation, body weight did increase, but there were no
significant changes in muscle strength or functional capacity1106. The story is to date incomplete.
Exercise training has been described as inducing useful changes in body composition of people
with COPD, which is well-known in healthy individuals. Fifty patients were compared with 36
age-matched controls for initial body composition (BMI, FFM), and the 50 patients were enrolled
in intensive inpatients training over 8 weeks. Age and FFM predicted muscle / exercise function,
and PR induced increase in FFM, reduction in body fat, and improvements in exercise
performance and muscle strength out of proportion to the changes in body composition1107. The
authors concluded that exercise itself is anabolic.
NUTRITIONAL INTERVENTIONS
KEY POINTS
1)
Nutritional assessment to detect early loss of muscle
mass and nutritional advice are warranted but
unproven
2)
Nutritional interventions and exercise training may
provide complementary benefits
Comprehensive Pulmonary Rehabilitation
Pulmonary rehabilitation and cardiac rehabilitation are applied to two of the largest patient
populations with chronic disabling disease in the developed world – COPD, and coronary heart
disease. The goals are similar, namely improved functionality and confidence, with physical
reconditioning. However, physical training has different effects in the two patient populations. In
coronary heart disease increased aerobic capacity can be achieved, and this is a major contributor
to better exercise tolerance, whereas in COPD improvements in exercise tolerance are achieved
by better peripheral muscle work efficiency with little or no change in aerobic capacity1108. In this
trial, similar exercise sessions and nutritional advice were provided, with disease- and treatmentspecific education sessions, and for COPD patients breathing retraining. The exercise benefits
were reflected in better quality of life and reduced somatisation in both groups. While similarities
and overlaps exist in components of exercise training and psychosocial support between cardiac
and pulmonary rehabilitation, there are substantial differences in the style of exercise training as
well as in the emphasis of education and specific breathing strategies.
1106
Ferreira IM, Verreschi IT, Nery LE, et al. The influence of 6 months of oral anabolic steroids on body
mass and respiratory muscles in undernourished COPD patients. Chest 1998; 114:19-28
1107
Franssen FME, Broekhuizen R, Janssen PP, et al. Effects of whole-body exercise training on body
composition and functional capacity in normal-weight patients with COPD. Chest 2004; 125:2021-2028
1108
Milani RV, Lavie CJ. Disparate effects of out-patient cardiac and pulmonary rehabilitation programs on
work efficiency and peak aerobic capacity in patients with coronary disease or severe obstructive
pulmonary disease. J Cardiopulm Rehabil 1998; 18:17-22
132
It is important that pulmonary rehabilitation works in an environment of disease management and
patient support, with close liaison among all care providers and the patient. Clear goals should be
developed for each patient, communicated to the care providers, and reviewed regularly. Since
benefits wane after six months or so involvement in an exercise program should continue,
knowledge should be refreshed and updated regularly, and social support structures should be
encouraged. While the individual components have benefits, greater efficacy is derived from a
comprehensive integrated program.
Several systematic reviews or overviews reveal the weight of evidence in favour of
comprehensive pulmonary rehabilitation for moderate and severe COPD. Most of the benefits
have been observed in hospital-based programs, but there is increasing appreciation of the need to
develop rehabilitation in the community.
A critical review of comprehensive pulmonary rehabilitation
This review was published in 19991109, selected research papers from the previous 45 years that
demonstrated good patient and outcome descriptors, use of control groups, and use of adequate
statistical analyses for meta-analysis. Of 79 studies identified, 42 had inadequate controls while a
number of others had insufficient descriptions or lack of adequate exercise training, leaving 18
articles. Highly significant and homogeneous improvements in maximal exercise capacity and
walking distance were found for up to 9 months after comprehensive PR. There were also
homogeneous significant improvements in HRQoL, dyspnoea, fatigue, emotion and mastery. This
meta-analysis extended the findings of an earlier meta-analysis1110, though with some more
homogeneous results, notably in improved exercise capacity (influenced by starting spirometry
heterogeneity in the earlier paper).
Since the 1999 meta-analysis a number of randomised controlled and other trials have been
published. Griffiths1111 evaluated 200 patients with chronic disabling lung disease (a mix of
diagnoses, but mostly COPD) randomly assigned to outpatient comprehensive PR or a “usual
medical care” group. As a reflection of the severity of their conditions, 14 patients died before the
one-year follow-up, and for some patients data were incomplete. Intention-to-treat analysis,
however, showed significant treatment effects for all dimensions of generic and disease-specific
health status and for exercise capacity immediately after PR, still significant at one year. There
was also less hospitalisation and use of primary care resources over the year of observation.
Green1112 studied 44 patients with moderate COPD, randomised to either a condensed four-week
or a full seven-week program of comprehensive PR. There were statistically greater benefits
accrued over 7 weeks than over 4 weeks in HRQoL, with trends to more exercise capacity.
Finnerty1113 reported a randomised controlled trial of outpatient PR. There were 36 patients
randomised to the active group, who had a 2-hour education and 1-hour exercise training session
1109
Cambach W, Wagenaar RC. Koelman TW, et al. The long-term effects of pulmonary rehabilitation in
patients with asthma and chronic obstructive pulmonary disease: a research synthesis. Arch Phys Med
Rehabil 1999; 80:103-111
1110
Lacasse Y, Wong E, Guyatt GH, King D, et al. Meta-analysis of respiratory rehabilitation in chronic
obstructive pulmonary disease. Lancet 1996; 348:1115-1119
1111
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at I year of outpatient
multidisciplinary pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
1112
Green RH, Singh SJ, Williams J, Morgan MDL. A randomised controlled trial of four weeks versus
seven weeks of pulmonary rehabilitation in chronic obstructive pulmonary disease. Thorax 2001; 56:143145
133
twice a week for weeks as well as voluntary patient support group attendance and follow-up
exercise maintenance sessions at 8, 9, and 10 weeks. There were 29 controls who simply attended
weekly outpatient clinical reviews. HRQoL improved in the treatment group by well over the
“minimal clinical effect”, but did not change in the controls. Small but clinically significant
improvements were also seen in walking distance.
In New Zealand, Young1114 conducted an uncontrolled prospective longitudinal study of 51
patients with severe COPD enrolled in a “pragmatic” outpatient hospital-based PR program with
multidisciplinary education group sessions and progressive aerobic exercise training. Significant
improvements were seen in exercise capacity, perceived dyspnoea and HRQoL at 3 and 6 months
after the program. Further, there were reduced hospital bed-days and courses of oral
corticosteroids for exacerbations in the 6 months after completion than in the 6 months before PR.
Ries1115 compared comprehensive PR to education alone in 119 patients with COPD, with an
initial 8-week program followed by monthly sessions for one year in the comprehensive group,
and good follow-up was obtained over 4 years. Significant benefits were described for exercise
capacity, walking self-efficacy, and perceived breathlessness and fatigue at 2 months, with loss of
all but exercise endurance and walking self-efficacy by 18 months, and essentially no difference
between the groups by 2 years. Over 4 years there were no differences in survival, quality of life,
depression, or hospitalisation.
Guell1116 conducted a randomised controlled trial of outpatient comprehensive PR with 30 COPD
patients in the therapy group and 30 matched controls in a “usual care” group. By 3 months there
were significant differences in dyspnoea, fatigue and emotional function, which then declined
slightly by 2 years. There were reduced exacerbations in the PR group, but no differences were
seen in hospitalisation. Importantly, only three patients needed to be treated to achieve significant
benefit in HRQoL for one patient over 2 years.
These studies and others were included in a Cochrane Systematic Review1117. This identified a
further nine papers since the earlier review, and confirmed highly significant improvements in
mastery, fatigue, emotional function and dyspnoea. All outcomes were greater than the minimum
clinically relevant improvements, with the exception of emotional function. Maximum exercise
capacity evaluated by incremental treadmill ergometry was measured in fourteen trials (n=255
rehabilitation, n=233 usual care), but the effects were inconsistent and small. Functional exercise
capacity was measured in ten trials using the six-minute walk test (n=235 rehabilitation, n=219
1113
Finnerty JP, Keeping I, Bullough I, Jones J. The effectiveness of outpatients pulmonary rehabilitation
in chronic lung disease. A randomized controlled trial. Chest 2001; 119:1705-1710
1114
Young P, Dewse M, Fergusson W, Kolbe J. Improvements in outcomes for chronic obstructive
pulmonary disease (COPD) attributable to a hospital-based respiratory rehabilitation program. Aust NZ J
Med 1999; 29:59-65
1115
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic
and psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995;
122:823-832
1116
Guell R, Casan P, Belda J, Sangenis M, et al. Long-term effects of outpatients rehabilitation of COPD:
A randomised trial. Chest 2000; 117:976-983
1117
Lacasse Y, Brosseau L, Milne S, Martin S, et al. Pulmonary rehabilitation for chronic obstructive
pulmonary disease. Cochrane Database Syst Rev 2002; Issue 3.
134
controls). The weighted mean average was 49 metres, slightly less than the quoted minimum
clinically significant difference of 54 metres (96%CI=37-71 m)1118.
The findings from these reviews of effectiveness, and other observations of extended exercise
endurance1119, better self-efficacy for exercise1120, less dyspnoea with exertion1121, reduced
1123,1124
, reduced levels of anxiety1125, and better HRQoL
dependence1122, less depression
following comprehensive PR, indicate the superiority of this approach over single modality
therapy. The most recent systematic review of pulmonary rehabilitation has added another 9
randomised controlled trials to the original review (23 in total met inclusion criteria)1126.
Statistically and clinically significant improvements were confirmed for CRDQ domains of
dyspnoea, fatigue and mastery, while the improvements in 6-minute walk distance were
borderline (49 metres).
It is important to reiterate that COPD in particular is a multifactorial and systemic condition, and
it frequently coexists with other comorbid conditions1127,1128. These play a role in the poor
HRQoL seen in COPD patients1129, add to the exercise impairment1130, contribute to worse
survival, and help determine outcomes from PR1131.
After pulmonary rehabilitation patients should therefore have better capacity in many different
aspects, and be confident to monitor and manage their lung condition more effectively so that
they need to access emergency treatment only rarely, and their dependency level is reduced.
Pulmonary rehabilitation should enable patients to collaborate in a more informed manner with
1118
Redelmeier DA, Bayoumi AM, Goldstein RS, Guyatt GH. Interpreting a small difference in functional
status: the six-minute walking test in chronic lung disease patients. Am J Respir Crit Care Med 1997;
155:1278-1282
1119
Cockcroft AE, Saunders MJ, Berry G. Randomised controlled trial of rehabilitation in chronic
respiratory disability. Thorax 1981; 36:200-203
1120
Kaplan RM, Atkins CJ, Reinsch S. Specific efficacy expectations mediate exercise compliance in
patients with COPD. Health Psychol 1984; 3:223-242
1121
Reardon J, Awad E, Normandin E, et al. The effect of comprehensive outpatient pulmonary
rehabilitation on dyspnoea. Chest 1994; 105:1046-1052
1122
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at I year of outpatient
multidisciplinary pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
1123
Ojanen M, Lahdenso A, Laitinen J, Karvonen J. Psychosocial changes in patients participating in a
chronic obstructive pulmonary disease rehabilitation program. Respiration 1993; 60:96-102
1124
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic
and psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995;
122:823-832
1125
Withers NJ, Rudkin ST, White RJ. Anxiety and depression in severe chronic obstructive pulmonary
disease: the effects of pulmonary rehabilitation. J Cardiopulm Rehabil 1999; 19:362-365
1126
Lacasse Y, Brosseau L, Milne S, Martin S, et al. Pulmonary rehabilitation for chronic obstructive
pulmonary disease. Cochrane Database Syst Rev 2006; Issue 2
1127
Soriano JB, Visick GT, Muellerova H, et al. Patterns of comorbidities in newly diagnosed COPD and
asthma in primary care. Chest 2005; 128:2099-2107
1128
Sidney S, Sorel M, Quesenberry CP, et al. COPD and incident cardiovascular disease hospitalisations
and mortality. Kaiser Permanente Medical Care Program. Chest 2005; 128:2068-2075
1129
Wijnhoven HA, Kriegsman DM, Hesselink AE, et al. The influence of comorbidity on health-related
quality of life in asthma and COPD patients. Respir Med 2003; 97:468-475
1130
Roomi J, Jonson MM, Waters K, et al. Respiratory rehabilitation, exercise capacity and quality of life
in chronic airways disease in old age. Age Ageing 1996; 25:12-16
1131
Crisafulli, Costi S, Luppi F, et al. Role of comorbidities in a cohort of patients with COPD undergoing
pulmonary rehabilitation. Thorax 2008; 63:487-492
135
their doctor and other health care providers in planning their own care. Their spouse or carers
should also feel more confident and less restricted. Most of these outcomes have not been
evaluated in controlled trials.
4.3 Health Economics and Pulmonary
Rehabilitation
The economics of health care are quite different in different countries, and firm conclusions for
Australia about costs of a complex treatment modality like rehabilitation are hard to draw from
research performed overseas. It has become possible only in the last decade to attach dollar
benefits to burden of illness or to gains in HRQoL, so that true cost-benefit analysis for
treatments that do not affect impairments while improving disability is a very recent science. It is
not surprising that there is very little information about cost-benefit of pulmonary rehabilitation in
the world literature.
Guidelines of pulmonary rehabilitation have given little attention to health economics, and studies
from one country are readily generalisable due to different funding and administrative
arrangements. The American guidelines1132 only addressed health care utilisation, and concluded
that there was insufficient information even about this component of economic analysis. They
identified eight observational studies and two non-randomised controlled trials1133,1134, which until
1997 had suggested pulmonary rehabilitation resulted in reduced numbers of hospital admissions
as well as reduced hospitalisation days following PR. One randomised controlled trial that
addressed these issues showed non-significant differences1135, and another showed significantly
reduced numbers of hospital admissions in 6 months after PR compared to usual care1136. The
European guidelines in 19971137 did not address themselves to health economics, while the British
guidelines1138 (2001) briefly commented on costs for programs, and made the statement “The
complete impact of rehabilitation on the lives of patients and their relatives is largely unexplored
and the health economic issues are currently being addressed”. Neither the 1997 nor the 2002
meta-analyses of components of PR1139,1140 examined health economics. The most recent joint
1132
AACVPR/ACCP Pulmonary Rehabilitation Guidelines Panel. Pulmonary Rehabilitation. Joint
ACCP/AACVPR evidence-based guidelines. Chest 1997; 112:1363-1396
1133
Sneider R, O’Malley JA, Kahn M. Trends in pulmonary rehabilitation at Eisenhower Medical Center:
an 11-years’ experience (1976-1987). J Cardiopulm Rehabil 1988; 8:453-461
1134
Lewis D, Bell SK. Pulmonary rehabilitation, psychosocial adjustment, and use of healthcare services.
Rehabil Nurs 1995; 20:102-107
1135
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic
and psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995;
122:823-832
1136
Jensen PS. Risk, protective factors, and supportive interventions in chronic airway obstruction. Arch
Gen Psychiatry 1983; 40:1203-1207
1137
Donner CF, Muir JF. Selection criteria and programmes for pulmonary rehabilitation in COPD patients.
Eur Respir J 1997; 10:744-757
1138
British Thoracic Society Standards of Care Subcommittee on Pulmonary Rehabilitation. “Pulmonary
rehabilitation”. Thorax 2001; 56:827-834
1139
Lacasse Y, Guyatt GH, Goldstein RS. The components of a respiratory rehabilitation program: a
systematic overview. Chest 1997 111:1077-1088
1140
Lacasse Y, Brosseau L, Milne S, Martin S, et al. Pulmonary rehabilitation for chronic obstructive
pulmonary disease. Cochrane Database of Systematic Reviews 2002; Issue 3
136
ATS/ERS statement on PR1141 does address health care utilization, but conclude further research
is needed to examine the health economic impacts long term of PR.
In 1997 a prospective randomised controlled study of the costs of a two-month inpatient PR
program in Ontario was reported in terms of HRQoL, from which a cost-effectiveness ratio was
derived 1142. The numbers needed to treat with PR to achieve a clinically significant improvement
in HRQoL was also determined from multiplying the incremental cost of providing PR over usual
care by the numbers needed to treat to calculate cost-effectiveness. This expensive inpatient
program had an incremental cost of CDN$11,597 per patient per year, but only 2.5 patients
needed to be treated to improve one patient’s mastery, or 4.4 patients to improve one patient’s
fatigue. To put these costs in perspective, a US pharmaco-economic analysis of the costs of
providing treatment for COPD found Stage III (severe) COPD costed on average US$10,812 per
patient per year1143.
In a randomised controlled trial no advantage in numbers of hospital admissions after PR could
be found over the control group, but reduced lengths of stay per admission in the PR group1144.
There was overall incremental cost effectiveness from adding comprehensive outpatient PR to
usual care in a randomised controlled trial, using the utility in terms of changes in qualityadjusted life years (QALYs) based on the SF-36, and a “bootstrapping” analysis to determine
whether societal or health administrators’ preferences were met. The program “produced cost per
QALY ratios within bounds considered to be cost effective and…likely to result in financial
benefits to the health service” 1145.
In a recent review of health economics in COPD, Halpin based most of his analysis on UK
calculations1146. He demonstrated that costs of COPD increase with severity of disease (₤781 to
₤1,154 per patient per year). He also referred to the estimate of cost-utility of PR, being ₤2,000 to
₤6,000 per QALY1147, and the high level of cost-effectiveness of this intervention. Work still
needs to be done on incremental cost-effectiveness of PR in Australia.
4.4 Shared care and self-management
People exhibit a range of capacities to self-manage, and the factors predicting their levels of selfmanagement behaviour can be explained by theoretical models. These models of coping with
1141
Nici L, Donner C, Wouters E, ZuWallack R, et al, on behalf of the ATS/ERS Pulmonary Rehabilitation
Writing Committee. American Thoracic Society/European Respiratory Society Statement on Pulmonary
Rehabilitation. Am J Respir Crit Care Med 2006; 173:1390-1413
1142
Goldstein RS, Gort EH, Guyatt GH, Feeny D. Economic analysis of respiratory rehabilitation. Chest
1997; 112:370-379
1143
Hilleman DE, Dewan N, Malesker M, Friedman M. Pharmacoeconomic evaluation of COPD. Chest
2000; 118:1278-1285
1144
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at I year of outpatient
multidisciplinary pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
1145
Griffiths TL, Phillips CJ, Davies S, et al. Cost effectiveness of an outpatient pulmonary rehabilitation
programme. Thorax 2001; 56:779-784
1146
Halpin DMG. Health economics of chronic obstructive pulmonary disease. Proc Am Thorac Soc 2006;
3:227-233
1147
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at I year of outpatient
multidisciplinary pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
137
chronic illness in general1148, or specifically with COPD1149, are complex in that they incorporate
interactions among a range of physical, psychological, medical and demographic variables. The
primary aim of these models is to identify the variables related to how patients deal with their
illness, and to use the knowledge to predict and manipulate the relationships among illness
perceptions, coping strategies and bio-psycho-social outcomes.
Behaviour change
For patients to change health-related behaviour they do need knowledge, yet provision of
knowledge alone has little effect on health behaviour1150. Instead, knowledge needs to be
supported by behavioural approaches, in which patients learn, practice and rehearse strategies that
lessen the impact of the illness, and from this they can develop the self-confidence (self-efficacy)
to self-manage1151,1152. It is important, too, that the patient’s medical attendants have skills and
understanding in sharing care with the patient. The doctor and other health professionals involved
in this care partnership need effective communication skills (for listening to their patients as well
as educating them). Training programs to enhance such capabilities can improve their patients’
health outcomes, at least in asthma, hypertension and the paediatrics areas1153,1154,1155.
Chronic disease self-management programmes
CDSMPs were developed for the purpose of reducing the morbidity and economic burden
associated with chronic disease and improving patient HRQoL1156,1157,1158. The aim of CDSMPs is
to disseminate a range of evidence-based interventions to a specific medical population to assist
with coordination of disease management and improve quality of care. The multi-factorial
components of CDSMPs include supporting the physician or practitioner/patient relationship and
plan of care, emphasizing the need for accurate diagnosis (including systemic effects and
comorbidities), symptom control, better functioning, and prevention of exacerbations and
complications. These goals are underpinned by evidence-based practice guidelines and patient
empowerment strategies, and achievement of goals is evaluated using clinical, humanistic, and
economic outcomes1159. CDSMPs have been developed for a variety of medical populations and
1148
Maes S, Leventhal H, de Ridder DTD. Copping with chronic diseases. In: Zeidner M, Endler NS, Eds.
Handbook of Coping: Theory, Research, Applications. New York, NY: John Wiley & Sons 1996: xxi
1149
Scharloo M, Kaptein AA, Weinman JA, et al. Physical and psychological correlates of functioning in
patients with chronic obstructive pulmonary disease. J Asthma 2000; 37:17-29
1150
Becker MH. Patient adherence to prescribed therapies. Med Care 1985; 23:539-555
1151
Bandura A. Social foundations of thought and action: a social cognitive theory. Englewood Cliffs, NJ:
Prentice-Hall, 1986
1152
Clark NM, Starr NS. Management of asthma by patients and families. Am J Respir Crit Care Med
1994; 149:S54-S66
1153
Clark NM, Gong M, Schork MA, Kaciroti N, et al. Long-term effects of asthma education for
physicians on patient satisfaction and use of health services. Eur Respir J 2000;16:15-21
1154
Inui TS, Yourtee EL, Williamson JW. Improving outcomes in hypertension after physician tutorials.
Ann Intern Med 1976; 84:646-651
1155
Maiman LA, Becker MH, Kiptak GS, et al. Improving pediatricians' compliance-enhancing practices: a
randomized trial. Am J Dis Child 1988; 142:733-779
1156
Wagner EH, Austin BT, Von Koroff M. Improving outcomes in chronic illness. Manag Care Q
1996;4:12-24
1157
Tsai AC, Morton SC, Mangione CM, et al. A meta-analysis of interventions to improve care for chronic
illnesses. Am J Man Care 2005;11:478-488
1158
Stuart M, Weinrich M. Integrated health system for chronic disease management: lessons learned from
France. Chest 2004;125:695-703
1159
Disease management association of America. DMAA definition of disease management (online).
Available from http://www.dmaa.org/dm_definition.asp (Accessed 10th August 2007)
138
implemented in a wide range of clinical and primary care settings, and are based on one of four
models.
(1) The Stanford Model utilizes peer educators in a structured group setting to help patients learn
the skills and strategies of disease self-management1160.
(2) The PRECEDE- PROCEED Model uses a nine-step process to first identify population
health needs, resource enabling factors and barriers, and then implement and evaluate the
program1161.
(3) The Chronic Care Model identifies the elements for an effective system-based model for
chronic disease management, including patient self-management support, clinical information
systems, delivery systems and healthcare and community resources1162,1163,1164,1165.
(4) Underpinned by CBT principles, the Flinders Model can be used for any psychiatric or
medical condition with comorbidities through the provision of a structured, patient-centred
framework in which interventions are tailored to patient needs and priorities identified with the
individual1166. Clinically important patient benefits have been reported from CDSMPs in a variety
of chronic diseases including asthma1167. Most CDSMPs focus upon physiologic outcomes in
patients with chronic conditions1168, but improved mental health outcomes have also been shown
following CDSMPs in patients with depression1169,1170 and anxiety1171.
Self-Management and Medical Management may not at first glance appear to be
complementary1172, but collaborative care that includes training and support of health providers,
1160
Lorig KR, Sobel DS, Stewart AL, et al. Evidence suggesting that a chronic disease self-management
program can improve health status while reducing hospitalization: a randomized trial. Med Care
1999;37:5-14
1161
Green WL, Kreuter WM. Health Promotion Planning: An Educational and Ecological Approach.
Mountain View; Mayfield Publishing Company:1999
1162
Wagner EH, Austin BT, Von Koroff M. Organizing Care for Patients with Chronic Illness. Milbank Q
1996;74:511-44
1163
Wagner EH, Austin BT, Davis M, et al. Improving chronic illness care: translating evidence into action.
Health Affairs 2001;20: 64-78
1164
Bodenheimer T, Wagner EH, Grumback K. Improving primary care for people with chronic illness.
JAMA 2002;288:1775-1759
1165
Bodenheimer T, Wagner EH, Grumback K. Improving primary care for people with chronic illness: the
chronic care model, Part 2. JAMA 2002; 288:1909-1914
1166
Battersby, MW, Higgins P, Collins J, et al, Partners in Health: The development of self-management for
SA HealthPlus participants. The Australian Coordinated Care Trials - Recollections of an Evaluation.
Canberra, Publications Production Unit, Commonwealth Department of Health and Ageing, 2002
1167
Gibson PG, Powell H, Coughlan J, et al. Self-management education and regular practitioner review for
adults with asthma (Cochrane Review). The Cochrane Library, Issue 1. Chichester, UK: John Wiley &
Sons, 2003
1168
Chodosh J, Morton SC, Mojica W, et al. Meta-analysis: chronic disease self-management programs for
older adults. Annals Intern Med 2005;143:427-438
1169
Neumeyer-Gromen A, Lampert T, Stark K et al. Disease management programs for depression; a
systematic review and meta analysis of randomized trials. Med Care 2004;42:1211-21
1170
UnГјtzer J, Katon W, Callahan CM, et al. Collaborative care management of late-life depression in the
primary care setting. JAMA 2002;288:2836-2845
1171
Rollman BL, Belnap BH,, et al. A randomized trial to improve their quality of treatment for panic and
generalized anxiety diorders in primary care. Arch Gen Psychiatry 2005;62:1332-41
1172
Gruman J, Von Korff M. Self-management services. Their role in disease management. Dis Manage
Hlth Outcomes 1999; 6:151-158
139
patients and carers improves outcomes across a range of chronic conditions1173. The Stanford
Model has been at the forefront of self-management programs aiming at people with a range of
chronic conditions1174, targeting ability to deal with frustration, fatigue and pain, exercise
programs, correct medication use, communication, nutrition and evaluation of treatments.
Significant improvements have been described for participants’ exercise, cognitive symptom
management, communication with doctors, self-reported general health, health distress, fatigue,
disability management and social role activities. In diabetes, for example, patients perceived
greater sense of control over their condition1175,1176 and hence better glycaemic control. The
programs are well-suited to community-based care as they often employ trained lay-leaders.
Self-management features extensively in the management of asthma. Specific education
programs and supports demonstrate better knowledge about asthma, reduced hospitalisation and
better health-related quality of life in randomised and controlled trials lasting for up to one
year1177,1178,1179,1180,1181,1182,1183,1184. A systematic review has analysed the benefits noted in the
fifteen trials meeting inclusion criteria for asthma self-management1185. More intensive training of
patients in how to adjust medications was more effective in changing behaviour and reducing
health care costs.
Based on these successes in non-respiratory and asthma areas, self-management was suggested as
a specific strategy for COPD1186, and results of such approaches have recently been reported.
Medication adjustment in addition to usual GP care has been compared to usual GP care in a
1173
Von Korff M, Gruman J, Schaefer J, et al. Collaborative management of chronic illness. Ann Intern
Med 1997; 127:1097-1102
1174
Lorig KL, Sobel DS, Stewart AL, Brown BW, et al. Evidence suggesting that a chronic disease selfmanagement program can improve health status while reducing hospitalisation – A randomised trial. Med
Care 1999; 37:5-14
1175
Halford WK, Goodall TA, Nicholson JM. Diet and diabetes (II): A controlled trial of problem solving
to improve dietary self-management in patients with insulin dependent diabetes. Psychol Health 1997;
12:231-238
1176
Howorka K, Pumprla J, Wagner-Nosiska D, Grillmayr H, et al. Empowering diabetes out-patients with
structured education: Short-term and long-term effects of functional insulin treatment on perceived control
over diabetes. J Psychosom Res 2000; 48:37-44
1177
Boulet L-P, Boutin H, Cote J, et al. Evaluation of an asthma self-management program. J Asthma 1995;
32:199-206
1178
Allen RM, Jones MP, Oldenburg B. Randomised trial of an asthma self-management program for
adults. Thorax 1995; 50:731-738
1179
D’Souza W, Burgess C, Ayson M, Crane J, et al. Trial of a “credit card” self-management plan in a
high-risk group of patients with asthma. J Allergy Clin Immunol 1996; 97:1085-1092
1180
Kotses H, Stout C, McConnaughy K, et al. Evaluation of individualized asthma self-management
programs. J Asthma 1996; 33:113-118
1181
Gibson PG, Coughlan J, Wilson AJ, Abramson M, et al. Self-management education and regular
practitioner review for adults with asthma. Cochrane Database of Sys Rev 2002; Issue 2
1182
Gallefoss F, Bakke DM. Cost-effectiveness of self-management in asthmatics: a 1-year follow-up
randomized, controlled trial. Eur Respir J 2001; 17:206-213
1183
Cote J, Bowie DM, Robichaud, Parent JG, et al. Evaluation of two different educational interventions
for adult patients consulting with an acute asthma exacerbation. Am J Respir Crit Care Med 2001;
163:1415-1419
1184
Ghosh CS, Ravindran P, Joshi M, Stearns SC. Reductions in hospital use from self management
training for chronic asthmatics. Soc Sci Med 1998; 46:1087-1093
1185
Powell H, Gibson PG. Options for self-management education for adults with asthma. Cochrane
Database Syst Rev 2006; Issue 4
1186
Worth H. Self management in COPD: One step forward? Patient Educ Counsel 1997; 32 (Suppl 1):
S105-S109
140
randomised controlled trial, with significant improvements seen in initiation of medications for
increased symptoms and correct antibiotic use1187. A similar study of patients with asthma and
COPD also found significantly fewer GP visits and better health-related quality of life in the
intervention group1188. Whether this single dimension of medication self-management, which is
so important in asthma, can be translated to other aspects of self-management was examined in a
large prospective randomised controlled study. After one year the patients with asthma who had
received the comprehensive self-management training had significantly more perceived control
and self-confidence regarding their asthma, though there were no significant improvements in
clinical outcomes1189.
Several CDSMPs have been trailed with COPD patients. Some studies found that CDSMPs
reduced the frequency or length of hospitalisations1190,1191,1192,1193, and were cost effective1194
while others found little evidence of their effectiveness1195,1196,1197. A systematic review in 2003
concluded that, due to the paucity of good quality studies there was a need for further research on
the efficacy of CDSMPs for patients with COPD in well-designed trials1198. Moreover, several
authors concluded that the inclusion of a mental health component may be critical to the
effectiveness of CDSMPs for COPD patients1199,1200,1201,1202,1203. Importantly, mental health issues
1187
Watson PB, Town GI, Holbrook N, Dwan C, et al. Evaluation of a self-management plan for chronic
obstructive pulmonary disease. Eur Respir J 1997; 10:1267-1271
1188
Gallefoss F, Bakke PS, Rsgaard PK. Quality of life assessment after patient education in a randomized
controlled study on asthma and chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999;
159:812-817
1189
Lorig K, Holman H, Sobel D. Living a Healthy Life With Chronic Conditions. Palo Alto, California:
Bull Publishing Co 1994
1190
Pushparajah S, McClellan R, Henry A, et al. Use of a chronic disease management programme in
COPD to reduce hospital admissions. Chron Respir Dis 2006;3:187-193
1191
Casas A, Troosters T, Gadoury MA, et al. Self-management reduces both short-and long-term
hospitalization in COPD. Eur Respir J 2005:26;853-857
1192
Bourbeau J, Julien M, Maltais F, et al. Reduction of hospital utilization in patients with chronic
obstructive pulmonary disease: a disease-specific self-management intervention. Arch Intern Med
2003;163;585-591
1193
Poole PJ, Chase D, Frankel A, et al. Case management may reduce the length of hospital stay in
patients with recurrent admission for chronic obstructive pulmonary disease. Respirology 2001;6:37-44
1194
Bourbeau J, Collet JP, Schwartzman K, et al. Economic benefits of self-management education in
COPD. Chest 2006;130:1704-1711
1195
Taylor SJC, Candy B, Bryer RM, et al. Effectiveness of innovations in nurse led chronic disease
management for patients with chronic obstructive pulmonary disease: a systematic review of the evidence.
BMJ, doi:10.1136/bmj.38512.664167.8K (published 10 August 2005)
1196
Martin IR, McNamara D, Sutherland FR, et al. Care plans for acutely deteriorating COPD: a
randomized controlled trial. Chron Respir Dis 2004;1:191-195
1197
McGeoch GR, Willsman KJ, Dowson CA, et al. Self-management plans in the primary care of patients
with chronic obstructive pulmonary disease. Respirology 2006;11:611-618
1198
Monninkhof EM, van der Valk PD, van der Palen J, et al. Self management education for chronic
obstructive pulmonary disease (Cochrane Review). The Cochrane Library, Issue 1. Chichester, UK: John
Wiley & Sons, 2003
1199
Adams, SG, Smith PK, Allan PF, et al. Systematic review of the chronic care model in chronic
obstructive pulmonary disease prevention and management. Arch Intern Med 2007;167:551-561
1200
Tsai AC, Morton SC, Mangione CM, et al. A meta-analysis of interventions to improve care for chronic
illnesses. Am J Man Care 2005;11:478-488
1201
Coultas D, Frederick J, Barnett B, et al. A randomized trial of two types of nurse-assisted home care for
patients with COPD. Chest 2005:128:2017-2024
1202
Wall MP. Predictions of functional performance in community-dwelling people with COPD. J Nurs
Scholash 2007;39:222-8
141
may affect the ability of patients to manage their illness. For example, self-management
knowledge that patients can achieve when well not infrequently breaks down during severe
exacerbations if they have significant tendency to panic1204. A small qualitative study reported
that COPD patients supported the use of CDSMPs, but believed that they should be
individualized and include strategies for addressing anxiety and depression1205. Dyspnoeic people
with COPD who used self-management strategies that focussed on easing dyspnoea during
activities (eg controlling overall movement or pacing – n=79) described lower levels of dyspnoea
intensity and dyspnoea distress1206. A prospective randomised trial in COPD patients (n=103)
comparing dyspnoea self-management (DSM), DSM plus four supervised exercise sessions, and
DSM plus 24 supervised exercise sessions found longer duration of exercise training was more
effective in controlling dyspnoea, but DSM alone also had positive effects on dyspnoea1207. Using
an expensive personalised self-management intervention for 191 patients with moderate and
severe COPD, a Canadian multicentre study showed significant reductions in hospital
admissions1208, though the main author acknowledges as well that further research is needed1209.
Home Care
Although the potential for home care of severe COPD exists, the evidence supporting its benefits
is not yet established in randomised controlled trials1210,1211,1212. The CHRONIC Program
(developed and evaluated in Spain and Belgium)1213,1214 is showing early promising results.
Nevertheless, because elderly people disabled by COPD actually receive fewer home supports,
such as direct and supportive nursing care and physiotherapy than similar-aged patients with
other disabling illnesses including Parkinson's disease, stroke, amputation or arthritis1215,
improvements may be more evident when inequities are redressed and specific patients in need
1203
Jordan N, Lee TA, Valenstein M, et al. Effect of care setting on evidence-based depression treatment
for veterans with COPD and comorbid depression. J Gen Intern Med 2007;Aug [Epub ahead of print]
1204
Dowson CA, Town GI, Frampton C, et al. Psychopathology and illness beliefs influence COPD selfmanagement. J Psychosom Res 2004;56:333-340
1205
Costi S, Brooks D, Goldstein RS. Perspectives that influence action plans for chronic obstructive
pulmonary disease. Can Respir J 2006;13:362-368
1206
Christenbery TL. Dyspnea self-management strategies: use and effectiveness as reported by patients
with chronic obstructive pulmonary disease. Heart Lung 2005; 34:406-414
1207
Carrieri-Kohlman V, Nguyen HQ, Donesky-Cuenco D, et al. Impact of brief or extended exercise
training on the Benefit of a dyspnea self-management program in COPD. J Cardiopulm Rehabil 2005;
25:275-284
1208
Bourbeau J, Julien M, Maltais F, et al. Reduction of hospital utilization in patients with chronic
obstructive pulmonary disease: a disease-specific self-management intervention. Arch Intern Med 2003;
163:585-591
1209
Bourbeau J. Disease-specific self-management programs in patients with advanced chronic obstructive
pulmonary disease: a comprehensive and critical evaluation. Dis Manage Hlth Outcomes 2003; 11:311-319
1210
Davies L, Wilkinson M, Bonner S, et al. “Hospital at home” versus hospital care in patients with
exacerbations of chronic obstructive pulmonary disease: prospective randomised controlled trial. BMJ
2000; 321:1265-1268
1211
Skwarska E, Cohen G, Skwarski KM, et al. Randomized controlled trial of supported discharge in
patients with exacerbations of chronic obstructive pulmonary disease. Thorax 2000; 55:907-912
1212
Ram FS, Wedzicha JA, Wright J, Greenstone M. Hospital at home for acute exacerbations of chronic
obstructive pulmonary disease. Cochrane Database Syst Rev 2003:CD003573
1213
Casas A, Troosters T, Garcia-Aymerich, et al. Integrated care prevents hospitalisations for
exacerbations in COPD patients. Eur Respir J 2006; 15:139-142
1214
Garcia-Aymerich J, Hernandez C, Alonso A, et al. Effects of an integrated care intervention on risk
factors of COPD readmission. Respir Med 2007; 101:1462-1469
1215
Yohannes AM, Roomi J, Connolly MJ. Elderly people at home disabled by chronic obstructive
pulmonary disease. Age & Ageing 1998; 27:523-525
142
are more effectively targeted. This approach, though, needs further careful analysis before it can
be recommended for widespread introduction.
A further intervention receiving interest, as technological advances in communication are
maturing, is that of the “telephone hotline”. This allows patients from their home to access
advice at any time of day or night, and its development has been supported by consumer focus
groups. One example (in Western Sydney), was evaluated over a 2-year observational period.
There were 675 calls made by 118 patients, 56% of calls being made “after hours”. It is at these
times that patients do not have access to their usual family doctor or consultant physician. In 12%
of cases hospital presentation was averted by advice given, and there were no adverse effects1216.
Pulmonary Rehabilitation involves a multi-disciplinary team, aims to enhance patient selfefficacy and to involve carers, and should have a clear commitment to quality improvement
through feedback and discussion with all people involved in the care of each patient. Despite
these intentions, no convincing evidence of better self-management has been shown in studies
that have examined this outcome1217,1218,1219,1220, though problems of statistical power and
experimental design limit the conclusions. PR and Patient Support Groups, however, are well
placed to provide training for patient self-management.
Expert Patients
Another option for SM training is to use lay leaders. The Stanford Model is an example of this
(see above). Another, derived from the Stanford Model, is the Expert Patients Program,
developed within the UK National Health Service Plan1221. A cost-effectiveness evaluation of the
EPP in chronic conditions (mostly endocrine and musculoskeletal problems) has been
reported1222. In this program patients self-referred from advertisements in GP surgeries and local
media. Patients attended six 2.5 hour group sessions weekly in groups of 8-12 led by patients who
already experienced long-term conditions and who had been trained and quality-controlled. Better
patient outcomes at slightly lower cost than patients in the six month waiting list control group.
Shared Care
Participation by primary care practitioners and specialist care physicians in providing planned
care programs for patients with chronic conditions, enabled by exchange of information has
become known as Shared Care. This has been shown effective in diabetes, but has been applied to
other conditions as well. There are several models:
1216
Roberts MM, Leeder SR, Robinson TD. Nurse-led 24-h hotline for patients with chronic obstructive
pulmonary disease reduces hospital use and is safe. Intern Med J 2008; 38:334-340
1217
Ojanen M, Lahdenso A, Laitinen J, Karvonen J. Psychosocial changes in patients participating in a
chronic obstructive disease rehabilitation program. Respiration 1993; 60:96-102
1218
Buchi S, Villiger B, Sensky T, Schwarz F, et al. Psychosocial predictors of long-term success on
inpatient pulmonary rehabilitation of patients with COPD. Eur Respir J 1997; 10:1272-1277
1219
Lox CL, Freehill. Impact of pulmonary rehabilitation on self-efficacy, quality of life, and exercise
tolerance. Rehabil Psychol 1999; 44:208-221
1220
Camp PG, Appleton J, Reid WD. Quality of life after pulmonary rehabilitation: Assessing change using
quantitative and qualitative methods. Physical Therapy 2000; 80:986-995
1221
Donaldson L. The expert patient: a new approach to chronic disease management for the 21st century.
Brit Med J 2003; 326:1279-1280
1222
Richardson G, Kennedy A, Reeves D, Bower P, Lee V, Middleton E, et al. Cost effectiveness of the
Expert Patients Programme (EPP) for patients with chronic conditions. J Epidemiol Community Health
2008; 62:361-367
143
Community Clinics
Specialists attend a clinic in the primary care setting with general practitioners and/or specialist
and/or GP practice nurses. Communication is not systematic, but may include a time for meeting
together to discuss cases.
Basic Shared Care model
Systematic communication is established between specialists and primary care practitioners, each
in their own environment, coordinated by an administrator.
A systematic review of these types of models concluded no recommendations could be made due
to under-powered studies and inconsistent outcomes being reported1223.
Liaison model
Liaison meetings are attended by primary care practitioners and specialists to discuss ongoing
management of registered patients.
Shared Care Record Card
A shared medical record is used by all primary care and specialist practitioners, and
communications made through this (usually patient-held) record.
Computer-Assisted Shared Care
An agreed data set is established to allow collection of common data, and access is provided
through a central repository as required by registered health professionals, and/or new
information additions are notified by email.
These three models were subjected to systematic review, with 19 randomised controlled trials
being identified. There were no consistent benefits in terms of physical or mental health,
disability measures, hospital admissions or satisfaction, but more consistent prescribing
(adherence with guidelines) was clearly evident1224.
4.5 Support Groups for Patients and Carers
In many chronic disease groups communal support (for both the patients and their families or
other carers) has proven helpful. The most common areas researched have been those relating to
cancer and psychosocial problems. Patients attending support groups (SG) scored lower on scales
of stress, confusion, fatigue and maladjusted coping responses and higher on a vigour index than
control group patients1225. As an active psychosocial intervention for cancer, community group
sessions for patients with metastatic breast cancer were evaluated1226. These groups were
educated about coping with their own symptoms and supporting their colleagues. Self-hypnosis
was taught for control of pain, and communication with health professionals or peers about their
1223
Gruen RL, Weeramanthri TS, Knight SE, Baillie RS. Specialist outreach clinics in primary care and
rural hospital settings. Cochrane Database Syst Rev 2003, Issue 4. Art No: CD003798
1224
Smith SM, Allwright S, O’Dowd T. Effectiveness of shared care across the interface between primary
and specialty care in chronic disease management. Cochrane Database Syst Rev 2007, Issue 3. Art No:
CD004910
1225
Spiegel D, Bloom JR, Yalom I. Group support for patients with metastatic cancer: a randomized
outcome study. Arch Gen Psychiatry 1981; 38:527-533
1226
Spiegel D, Bloom JR, Kraemer HC, Gottheil E. Effects of psychosocial treatment on survival of
patients with metastatic breast cancer. Lancet 1989; 14:888-891
144
fears was actively encouraged. This study showed a somewhat surprising significant
improvement in longevity as well as quality of life, and the effect has been replicated1227.
Group support has also developed in the fields of Dementia and Alzheimer’s disease,
schizophrenia and other mental illnesses, severe arthritis, asthma, cancer, and diabetes mellitus.
In many of these fields controlled trials have shown at least short-term benefits. For example,
male patients positive for HIV who were regular SG attendees reported lower levels of emotional
distress, used more effective coping strategies, and had higher perception of efficacy and control
than control group subjects1228. In an alcoholic population, SG attendance was the most powerful
predictor of treatment success1229. SG attendance has been found to reduce the number and
duration of hospitalisations in mentally ill patients1230. In many studies, however, longitudinal
data are not provided, and where such data do exist, they are less supportive of sustained benefit.
In COPD, there are no published randomised controlled trials of benefits from or costs of SGs. A
recent pilot study on recently discharged COPD patients found positive health outcomes from a
community intervention programme consisting of medical education and community and peer
support. There were improvement in symptoms, exercise tolerance, quality of life and of the
perceptions of illness, and the authors concluded that the group environment might reduce
depression and anxiety by improving self-efficacy or self-esteem through the provision of mutual
support1231.
In Australia, the Australian Lung Foundation’s LungNet has been a popular development among
its 8,000 or more members, in spite of a lack of efficacy shown in randomised controlled trials.
There are published abstracts from several controlled studies in Australia that mirror observations
made in other disease populations. These examined the psychological health and handicap of
carers of patients with COPD, and of changes in the handicap experienced by carers following
their patient’s involvement in PR and in SGs. The results showed similar psychological health
problems in caregivers of patients with chronic lung disease as in carers of other disease
populations, significant linkages between psychological health of carers and patients1232, a
reduction in their burden of care following PR or SG involvement1233,1234, and a shift in activities
between carers and patients (reflecting a reduction in patient dependence)1235,1236, suggesting that
SGs for COPD patients may be useful adjuncts to PR.
1227
Goodwin PJ, Leszcz M, Ennis M, Koopmans J, et al. The effect of group psychosocial support on
survival in metastatic breast cancer. New Engl J Med 2001; 345:1719-1726
1228
Fontaine KR, McKenna L, Cheskin LJ. Support group membership and perceptions of control over
health in HIV+ men. J Clin Psychol 1997; 53:249-252
1229
Miller NS, Ninonuevo FG, Klamen DL, et al. Integration of treatment and posttreatment variables in
predicting results of abstinence-based outpatient treatment after one year. J Psychoactive Drugs 1997;
29:239-243
1230
Lustig SL, Malomane E, Tollman S. A support group for mentally ill people. World Health Forum
1997; 18:319-322
1231
Woo J, Chan W, Yeung F, et al. A community model of group therapy for the older patients with
chronic obstructive pulmonary disease: a pilot study. J Eval Clin Pract. 2006;12:523-531
1232
Cafarella P, Frith P. Psychological status of COPD Patients and their carers are linked. Respirology
2001; 6 (Suppl):A36
1233
Cafarella P, Frith P. Pulmonary Rehabilitation reduces carer strain and psychological morbidity.
Respirology 2000; (Suppl: A43
1234
Cafarella P, Frith P. Patient completion of pulmonary rehabilitation reduces carer handicap.
Respirology 2001; 6 (Suppl):A35
1235
Cafarella P, Frith P. Benefits of Lung-Net support group membership. Respirology 2002; 7 (Suppl):A33
1236
Cafarella P, Frith P. Carers assessment of patient social adjustment following pulmonary rehabilitation.
Respirology 2001; 6 (Suppl):A12
145
It seems logical to encourage patients and their carers to attend SGs for social support also to
receive continued reminders of the benefits of activities and good nutrition. It also appears logical
to recommend SG membership as a standard follow-on from attendance at a PR program. These
recommendations are to date unsupported by evidence in respiratory disease. If such
recommendations are followed, though, attention should be given to aligning the information and
activities of the SG with those of the PR program.
4.6 Staffing for Pulmonary Rehabilitation
Over the thirty-five years in which formal PR programs have been operating, a range of
professionals have contributed to the programs and their evolution. In the US, for example,
respiratory therapists were lead professionals, with exercise physiologists and other respiratory
scientists, respiratory internists (physicians), specialists nurses, physiotherapists and mental
health workers adding expertise in various quanta at different times. It is clear that in Australia
physiotherapists have established many programs, initially for exercise training, and often based
on cardiac rehabilitation experiences. Specialist nurses have emerged within the past 20 years,
and have increasingly played primary roles in PR programs, particularly contributing an
education emphasis. Expert assistance has been recruited from respiratory scientists and from
other allied health professionals. It has only been in the past 10 years, however, that respiratory
physicians have widely acknowledged the value of PR, and many have now assumed either
supportive or organisational roles. Community health workers have begun to make a contribution,
especially since coordinated and integrated care have become more interesting to system
managers. An emerging professional group, especially in cardiac rehabilitation, is from the
exercise science stream.
At the outset, it should be said that there is no single best staffing structure. There is essentially
no evidence base for recommending any particular craft group’s central role, involvement or
exclusion. It is not the intention of this document to provide credentials or the basis of a
credentialing process. Indeed, local needs will inevitably dictate local solutions. However, there
are some principles that administrators and all staff need to acknowledge, and this Chapter aims
to clarify these.
The definitions of PR emphasise the importance of multidisciplinary inputs, integration of
services and goals of service provision1237,1238
The issues that impact on the patient with a chronic respiratory condition, and on the carer,
largely dictate the range of services that need to be provided, and the personnel who logically
should be involved in delivering the outcomes. Local needs and limitations will influence who
can deliver the basic information package and even who supervises exercise training. In a
regional centre, for example, a PR program may be coordinated by a community nurse, who may
also provide the entire education program, perhaps with help from a local pharmacist, GP and
mental health worker. Aboriginal health workers can also provide a culturally-tailored PR
program. An exercise training program in the community setting could be organised and
1237
Fishman AP. NIH Workshop summary. Pulmonary rehabilitation research. Am J Respir Crit Care Med
1994; 149:825-833
1238
AACVPR/ACCP Pulmonary Rehabilitation Guidelines Panel. Pulmonary Rehabilitation. Joint
ACCP/AACVPR evidence-based guidelines. Chest 1997; 112:1363-1396
146
supervised by exercise scientists and/or physiotherapists. Medical knowledge could be delivered
by a GP, a respiratory physician, a nurse or respiratory educator, and information on how to use
respiratory medications could be delivered by a doctor, pharmacist or respiratory educator.
Staffing Philosophies
Whoever establishes and coordinates a PR program, and whatever staff they employ, need to
understand the philosophy of PR and the needs of the participants. Above all staff should be
enthusiastic, motivated and committed to patient well-being, which is, after all, the prime goal of
PR. They should appreciate that chronic respiratory diseases are complex and are associated with
an extraordinary range of non-respiratory issues, of medical, psychological and social nature.
There is nothing wrong with being excited with an individual patient's achievements arising from
their membership of a group, or with being at all times optimistic in the face of apparent failure.
Small gains to a therapist can represent enormous accomplishment to a highly disabled patient, or
to an over-burdened carer.
It is all too easy for an interdisciplinary program to begin to believe that staff or structure are the
reasons for being. It must always be remembered that the program exists for the patient, and that
it is part of that patient's continuum of treatment and even of life experience.
Full-time staff and contributing providers should have an understanding of the role of PR in
overall disease management, and some appreciation of health economic issues. They need to be
committed to performance development and continuous improvement, to be aware of their own
roles and responsibilities, the role and responsibilities of their colleagues and the participants, and
the overlapping and interacting nature of these roles and responsibilities.
In an ideal interdisciplinary environment the priority should be the team, and professional or
personal jealousies are unnecessary. On the other hand, team leaders need to recognise the
professional knowledge, experience and skills each team member brings to the program, and team
members should acknowledge each other's contributions to the collective knowledge.
Communication is essential for good team management and quality improvement, and should be
given high priority.
Structure
The structure of a PR program team is subordinate to its function and philosophies. However,
some structure will be required to sure the function and philosophies are followed.
Program Director
Any team needs a captain at the very least. The professional heading the team should have a
substantive time commitment to the role, and have sufficient knowledge and experience to
understand the special attributes of patients with chronic and complex respiratory disease, their
carers, and the therapists on the team. An appreciation of and preferably a role within the overall
organisation of respiratory services in the region is also necessary. In large hospitals the Program
Director may be a respiratory physician, a nurse manager, or a senior allied health professional. In
a community or regional centre, a similar spectrum of staff may aspire to such a position, but a
senior administrator may also possess many of the required attributes. The Program Director and
Medical Director may be one and the same person.
147
The Program Director is administratively and professionally responsible for the efficient running
of the program. He/she will therefore supervise budgets, staffing issues, plant, equipment,
consumables, the setting and reviewing of policies and program goals, communication within the
team and from the members of the program, and ensure that the program fits well with other
elements of the care continuum.
Medical Director
Sometimes the Program Director will also be the Medical Director. The Medical Director is a
vital link to the medical profession. He/she is responsible for informing doctors in all health
sectors of the benefits, costs and positioning of PR, recommending strategies for patient
involvement, ensuring good medical care in continuity with primary care and specialists,
maintaining high quality information relating to evidence-based best practice, and ensuring other
health professionals understand chronic complex respiratory diseases and their management.
The Medical Director of a Comprehensive PR Program should be a fully qualified Respiratory
Physician, with experience in care of patients with chronic complex respiratory diseases, and
knowledge of respiratory physiology and exercise physiology.
Program Coordinator
A coordinator of activities is required. This may be an administrative/clerical officer or a health
professional. The Program Coordinator is responsible for ensuring that patients referred to the
program are enrolled for initial assessments, all elements of the program, and follow-up in a
timely fashion. Print materials and other educational aids need to be organised. A communication
stream between referring professionals or organisations and the PR program needs to be
maintained in full working order. The team members need to be informed about team meetings
and the times of their sessions in the program. Patient access needs to be facilitated, and carers
assisted where necessary. Above all, the Coordinator is often the public face of the program, and
needs to be well informed about the program, patient and compassionate.
Professional Team Members
As indicated above, there is a wide array of health professionals who may interact with patients
and be useful contributors to a PR program. They should all consider themselves to be teammembers and, as indicated, have a full understanding of and commitment to patient well-being
and the philosophies of the Pulmonary Rehabilitation.
The following professionals could be team members:
• Respiratory Physician
• General Physician
• General Practitioner
• Respiratory Nurse
• Community Nurse
• Pharmacist
• Respiratory scientist / technologist
• Exercise scientist
• Physiotherapist
• Occupational therapist
• Psychologist
148
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Psychiatrist
Mental health worker
Behavioural scientist
Volunteer coordinator
Community health worker
Social worker
Nutritionist
Dietician
Speech pathologist
Continence nurse
Palliative care nurse of physician
Chaplain / pastoral care associate
Vocational rehabilitation counsellor or therapist
Massage therapist
Home-care associate
There may be roles for other health or caring professionals as well, according to local custom or
availability. While there has been no acknowledgement of a role for volunteers in American
guidelines, it is very appropriate that volunteer workers could provide valuable input, especially
for carer support such as respite, social outing support, patient support group organisation, fundraising, and so on.
Communication
Members of the team can contribute best to the team approach if they are part of a
communication net. This applies equally to management, staff and consumers.
Regular meetings should be held (face-to-face or teleconferenced) which all team members
attend, with the prime purpose being review of the program. This may be twice a year. It may suit
some programs to have planning days off-site (eg every two years) to re-set goals, priorities,
policies, facilities, staffing structures, and other pertinent matters.
Meetings about individual patients or emergent program problems may be required ad hoc,
involving any combination of staff relevant to the problem. It may suit some programs to arrange
a regular meeting of an "executive group" to ensure problems about individual patients and
program matters are resolved in the most expeditious was possible.
All staff members need to maintain a strong commitment to free communication with patients and
their carers, both prospective and reactive. A telephone contact point needs to be agreed for these
consumers, and this may be the coordinator or one of the team members.
Results of initial assessments and of outcome measurements should be communicated to the
referring professional and others involved in the care of the patient as quickly as possible after the
results are tabulated. The Medical Director may need to append suggestions about ongoing
management. Any Action Planning done with the patient needs to be transmitted to the GP and
other vital care members, also in a timely way.
149
COMPREHENSIVE PULMONARY REHABILITATION
KEY POINTS
1)
Comprehensive PR is integrated inter-disciplinary treatment
2)
It should include exercise training, psychosocial support, and
education directed to behaviour change and self-management
3)
Nutritional advice and teaching breathing techniques may be
of additional help
4)
Comprehensive PR is highly effective and cost-effective for
improving functional status, exercise capacity and health
related quality of life for people with moderate to severe
COPD
5)
Clinically significant improvements in dyspnoea, fatigue and
mastery occur following programs that include exercise
training for at least 4 weeks
6)
Family caregivers are adversely affected by their spouse’s
COPD, and can be helped by the patient’s involvement in PR
7)
Support groups help to improve quality of life, and may
improve both patient and family caregiver
150
5. CLINICAL INDICATORS AND
OUTCOME MEASUREMENT
In this section, an attempt is made to provide an understanding of the type, derivation, meaning, validity
and application of particular indicators. Where possible, references are made to the uses of each indicator
in specific research studies, associations with other indicators and outcome measures and their
demonstrated or recommended clinical applications. There are several review documents that provide
useful perspectives on biomarkers1239, clinical indicators1240, and clinical outcomes1241,1242,1243,1244, and the
important properties of measurement tools to evaluate when deciding what to use1245.
5.1 Respiratory Symptoms
Patients undertaking therapeutic interventions often report changes in symptoms. In COPD the main
symptoms are dyspnoea (unpleasant or uncomfortable respiratory sensations, for which there may be
multiple descriptors1246), cough, and sputum production (a defining feature of Chronic Bronchitis).
Attempts made to standardise reporting of these symptoms have not given much attention to the
reproducibility or sensitivity of the instruments, particularly in COPD. The tools usually rely (inevitably)
on self-assessment and self-report, with inherent biases. Frequency or severity of coughing, and frequency,
amount and colour of sputum are dependent on a range of patient factors, with the psychological status1247
and cognitive capacity (notably verbal memory)1248 being major variants.
Dyspnoea
Chronic dyspnoea and pain are the two most universally disabling symptoms. They are initiated by a
variety of primary pathophysiologies, sensed by peripheral receptors, perceived centrally and interpreted,
then expressed behaviourally. In respiratory conditions dyspnoea is the chief symptom, experienced on a
daily basis by at least half those with COPD1249, and by virtually all COPD sufferers through any one year
of life1250. The inputs to perceived breathing discomfort are legion, and the interpretations of the sensation
1239
Barnes PJ, Chowdhury B, Kharitonov SA, Magnussen H, et al. Pulmonary biomarkers in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 2006; 174:6-14
1240
Jones PW, Agusti AGN. Outcomes and markers in the assessment of chronic obstructive pulmonary disease. Eur
Respir J 2006; 27:822-832
1241
Curtis JR, Martin DP, Martin TR. Patient-assessed health outcomes in chronic lung disease. What are they, how
do they help us, and where do we go from here? Am J Respir Crit Care Med 1997; 156:1032-1039
1242
Haughney J, Gruffydd-Jones K. Patients-centred outcomes in primary care management of COPD – what do
recent clinical trial data tell us? Prim Care Respir J 2004; 13:185-197
1243
Sullivan SD, Buist AS, Weiss K. Health outcomes assessment and economic evaluation in COPD: challenges and
opportunities. Eur Respir J 2003; 21 (Suppl 41):1s-3s
1244
Gross NJ. Outcome measures for COPD treatments: A critical evaluation. COPD 2004; 1:41-57
1245
Jones PW, Kaplan RM. Methodological issues in evaluating measures of health as outcomes for COPD. Eur
Respir J 2003; 21 (Suppl 41):13s-18s
1246
Elliott MW, Adams L, Cockcroft A, McRae KD, et al. The language of breathlessness: use of verbal descriptors
by patients with cardiorespiratory disease. Am Rev Respir Dis 1991; 144:826-832
1247
Dales RE, Spitzer WO, Schechter MT, Suissa S. The influence of psychological status on respiratory symptom
reporting. Am Rev Respir Dis 1989; 139:1459-1463
1248
Incalzi RA, Gemma A, Marra C, Capparella O, et al. Verbal memory impairment in COPD: Its mechanisms and
clinical relevance. Chest 1997; 112:1506-1513
1249
Rabe KF. Improving dyspnea in chronic obstructive pulmonary disease. Optimal treatment strategies. Proc Am
Thorac Soc 2006; 3:270-275
1250
Booth S, Wade R, Johnson M, Kite S, et al. Expert Working Group of the Scientific Committee of the
Association of Palliative Medicine. The use of oxygen in the palliation of breathlessness. Respir Med 2004; 98:66-77
151
vary widely1251,1252. The verbal descriptors used by patients for what they mean by dyspnoea are also very
1253, ,1254
, as is the recall patients have about the severity and frequency of their
individual
1255,1256
1257,1258
. Consequently, the evaluation of dyspnoea is complex
. Recent review have
dyspnoea
1259,1260
. Dyspnoea has been widely studied, using simple measures of
summarised these issues
performance dyspnoea, detailed analyses of baseline and changing dyspnoea, and characterisations of the
sensations of dyspnoea both at one time point and longitudinally. Dyspnoea ratings have correlated with
well being and HRQoL better than FEV11261. They appear to relate to COPD perceived severity and predict
survival better than traditional severity stages based on FEV11262,1263. The most widely used and tested
objective measures of dyspnoea are the Medical Research Council (MRC) Dyspnoea Scale, Oxygen Cost
Diagram (OCD), Modified Borg Score, visual analogue scales (VAS), Baseline and Transition Dyspnoea
Indexes (BDI/TDI), and scores for dyspnoea contained within HRQoL instruments (especially CRDQ –
see below). An analysis of outcome measures in an open study of comprehensive PR found that VAS at
peak exercise, MRC Grades, CRDQ Dyspnoea, and BDI/TDI functional indexes were highly responsive to
change after PR, with SGRQ symptom score being less responsive. However, there were close correlations
between the different dyspnoea indexes. The CRDQ and VAS at peak exercise were the most sensitive,
while BDI/TDI and MRC Scales were moderately sensitive1264.
MRC Dyspnoea Scale
Originally reported in 1960, this scale lists five grades of perceived disablement, taken directly from the
sensation of breathlessness felt by an individual during a range of typical daily activities1265,1266.
1251
Elliott MW, Adams L, Cockroft A, McRae KD, et al. The language of breathlessness: use of verbal descriptors by
patients with cardiopulmonary disease. Am Rev Respir Dis 1991; 144:826-832
1252
Rabe KF. Improving dyspnea in chronic obstructive pulmonary disease. Optimal treatment strategies. Proc Am
Thorac Soc 2006; 3:270-275
1253
Elliott MW, Adams L, Cockroft A, McRae KD, et al. The language of breathlessness: use of verbal descriptors by
patients with cardiopulmonary disease. Am Rev Respir Dis 1991; 144:826-832
1254
Scano G, Stendardi L, Grazzini M. Understanding Dyspnoea by its language. Eur Respir J 2005; 25:380-385
1255
Stulbarg MS, Carrieri-Kohlman V, Gormley JM, et al. Accuracy of recall of dyspnea after exercise training
sessions. J Cardiopulm Rehabil 1999; 19:242-248
1256
Meek PM, Lareau SC, Anderson D. Memory for symptoms in COPD patients: How accurate are their reports?
Eur Respir J 2001; 18:474-481
1257
Hajiro T, Nishimura K, Tsukino M, Ikeda A, et al. Analysis if clinical methods used to evaluate dyspnea in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 158:1185-1189
1258
Parshall MB. Psychometric characteristics of dyspnea descriptor ratings in emergency department patients with
exacerbated chronic obstructive pulmonary disease. Res Nursing Health 2002; 25:331-344 2002
1259
Rabe KF. Improving dyspnea in chronic obstructive pulmonary disease. Optimal treatment strategies. Proc Am
Thorac Soc 2006; 3:270-275
1260
Mahler DA. Mechanisms and measurement of dyspnea in chronic obstructive pulmonary disease. Proc Am
Thorac Soc 2006; 3:234-238
1261
Mahler DA, Faryniarz K, Tomlinson D, Colice GL, et al. Impact of dyspnea and physiologic function on general
health status in patients with chronic obstructive pulmonary disease. Chest 1992; 102:395-401
1262
Hajiro T, Nishimura K, Tsukino M, Ikeda A, et al. A comparison of the level of dyspnoea vs disease severity in
indicating the health-related quality of life of patients with COPD. Chest 1999; 116:1632-1637
1263
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
1264
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1265
Fletcher CM, Elmes PC, Fairbairn MB, et al. The significance of respiratory symptoms and the diagnosis of
chronic bronchitis in a working population. Br Med J 1959; 2:257-266
1266
Fletcher CM. Standardised questionnaire on respiratory symptoms: a statement prepared and approved by the
MRC Committee on the Aetiology of Chronic Bronchitis (MRC Breathlessness Score). Br Med J 1960; 2:1665
152
TABLE 5.1.
MRC Grade
Grade
Grade
Grade
Grade
0
1
2
3
Grade 4
1267
MODIFIED MEDICAL RESEARCH COUNCIL (MRC) DYSPNOEA SCALE
Activity causing breathing difficulty
I only get breathless with strenuous exertion
I get breathless hurrying on the level or walking up a slight hill
I have to walk more slowly than people my own age because of breathlessness
I have to stop for breath after walking around 100 metres on level ground or after
walking a few minutes on level ground
I am too breathless to leave the house because of breathing difficulty, or I get
breathless when dressing or undressing
The MRC Scale correlates well with the 12-minute walking distance1268, shuttle walk distance, SGRQ
Activity and Impacts Scales, and the CRDQ dimensions of Fatigue, Emotional Function and Mastery
Scores, but less well with spirometry (r= -0.42)1269. Surprisingly, MRC Grades do not correlate as well
with CRDQ Dyspnoea dimension, perhaps because each individual selects his/her own set of activities
causing breathlessness in the latter. MRC Grades also correlate with BDI focal score, as well as with each
component of BDI (r=0.61 to 0.74), and with the OCD (r=0.53 to 0.59)1270,1271.
This questionnaire is simple for the patient to answer as it is relevant to everyday activities, can be
completed in about 30 seconds and has excellent inter-observer agreement. It has been used to grade
clinical severity of COPD in rating impact of dyspnoea on HRQoL1272, and more effectively discriminated
prognosis/survival than FEV1 in a five-year observational study of 227 patients with COPD1273.
Subsequently it has been included as the dyspnoea rating tool with body mass index, FEV1 and 6-minute
walk distance in the BODE Index, which provides a high correlation with survival in moderate and severe
COPD1274. Although a rather coarse tool, in which a change in Grade by one is highly clinically relevant, it
is reasonably responsive to interventions such as PR (p=0.018), though less so than VAS after a 6-minute
walk test or BDI/TDI1275. MRC Scale is recommended by NICE and COPD-X guidelines for management
of COPD as a cross-sectional indicator of disease severity.
Oxygen Cost Diagram (OCD)
This measure was devised in an attempt to equate certain activities to their metabolic requirements1276.
Each stated activity is represented at intervals along a 100 mm line, and the individual is asked to indicate
with a mark on the line above the activities that most consistently would cause him/her to be breathless.
Like the MRC Scale, therefore the OCD provides an insight into the threshold of activities causing the
individual disabling breathlessness. The OCD has not been widely used as a clinical indicator of dyspnoea
or as an outcome measure. It does correlate well with MRC Grades (r=0.53) and BDI focal score (r=0.54)
1267
Fletcher CM. Standardised questionnaire on respiratory symptoms: a statement prepared and approved by the
MRC Committee on the Aetiology of Chronic Bronchitis (MRC Breathlessness Score). Br Med J 1960; 2:1665
1268
McGavin CR, Artvinli M, Naoe H, McHardy GJR. Dyspnoea, disability and distance walked: comparison of
estimates of exercise performance in respiratory disease. Br Med J 1978; 2:241-243
1269
Bestall JC, Paul EA, Garrod R, Garnham R, et al. Usefulness of the Medical Research Council (MRC) dyspnoea
scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 1999; 54:581-586
1270
Mahler DA, Wells CK. Evaluation of clinical methods for rating dyspnea. Chest 1988; 93:580-586
1271
Guyatt GH, Thompson PJ, Berman LB, Sullivan MJ, et al. How should we measure function in patients with
chronic heart and lung disease? J Chron Dis 1985; 38:517-524
1272
Hajiro T, Nishimura K, Tsukino M, Ikeda A, et al. A comparison of the level of dyspnoea vs disease severity in
indicating the health-related quality of life of patients with COPD. Chest 1999; 116:1632-1637
1273
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
1274
Celli BR, Cote CG, Mariv JM, Casanova C, et al. The BMI, airflow obstruction, dyspnea and exercise capacity
index in COPD. New Engl J Med 2004; 350:1005-1012
1275
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1276
McGavin CR, Artvinli M, Naoe H, McHardy GJR. Dyspnoea, disability and distance walked: comparison of
estimates of exercise performance in respiratory disease. Br Med J 1978; 2:241-243
153
and sub-elements of BDI (r=0.48 to 0.50), but less well with spirometry (r=0.16 to 0.48)1277. The OCD may
require careful explanation before completion, and takes one to two minutes to complete. Its clinical utility
has not been established.
Modified Borg Score
The development and methodology of this non-linear scale is based on psychophysical principles, and has
been widely used in exercise testing since its first description1278. It allows the patient to match the
perceived severity of symptoms or of effort with numbers on the scale1279, and directly indicates the
patient’s perceived dyspnoea (or other symptom) during a specified task. Scores can be indicated at
different workloads, though the score at maximum work is the most reproducible1280. Scoring requires brief
(but standardised) explanation before use, and standardised questions should be used each time. Each
estimate takes a few seconds. Scores are highly repeatable in the short term1281, but less so in the longer
term1282. The measure of exercise performance is more repeatable than the Borg rating at load1283, but Borg
Scores correlate well with magnitude of work performed and total ventilation1284. Responsiveness to
interventions like PR is not clear, though if measured at �isotime’ (i.e. the same time of serial exercise tests
regardless of the maximum load reached) use of tiotropium has been shown to reduce Borg Dyspnoea
significantly1285.
Visual Analogue Scale (VAS) at peak exercise
The VAS has been used in a variety of clinical settings since its first description in 19571286. Whereas the
Borg scale is non-linear and discontinuous, VAS is continuous and linear. It consists of a 100 mm line on
which the patient indicates a mark according to perceived breathing discomfort, with anchor points at each
end of nil and absolute maximum. It has been adapted for application at rest and end of exercise1287.
Baseline VAS is highly repeatable, but VAS during sub-maximal work is variable within subjects over the
medium term1288. VAS has been validated as a clinical indicator for COPD-related dyspnoea1289, and as an
outcome measure in a recent randomised controlled trial of opiates for dyspnoea, where it was found to be
repeatable and responsive to the intervention1290. Further, VAS at the end of a 6-minute walk test changed
significantly after completion of PR in an uncontrolled observational study of 37 patients with COPD1291.
1277
Mahler DA, Wells CK. Evaluation of clinical methods for rating dyspnea. Chest 1988; 93:580-586
Borg G. Psychophysical bases of perceived exertion. Med Sci Sports Exer 1982; 14:377-381
1279
Mador MJ, Rodis A, Magalang UJ. Reproducibility of Borg Scale measurements of dyspnoea during exercise in
patients with COPD. Chest 1995; 107:1590-1597
1280
Mador MJ, Rodis A, Magalang UJ. Reproducibility of Borg Scale measurements of dyspnoea during exercise in
patients with COPD. Chest 1995; 107:1590-1597
1281
Silverman M, Barry J, Hellerstein H, Janose J, Kelsen S. Variability of the perceived sense of effort in breathing
during exercise in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1988; 137:206-209
1282
Mador MJ, Rodis A, Magalang UJ. Reproducibility of Borg Scale measurements of dyspnoea during exercise in
patients with COPD. Chest 1995; 107:1590-1597
1283
Bestall JC, Paul EA, Garrod R, Garnham R, et al. Usefulness of the Medical Research Council (MRC) dyspnoea
scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 1999; 54:581-586
1284
Mahler DA. The measurement of dyspnea during exercise in patients with lung disease. Chest 1992; 101:242S247S
1285
O’Donnell DE, Fluge T, Gerken F, Hamilton A, et al. Effects of tiotropium on lung hyperinflation, dyspnoea and
exercise tolerance in COPD. Eur Respir J 2004; 23:832-840
1286
Stervus SS, Galunter EH. Ratio scales and category scales for a dozen perceptual continua. J Exper Psychol 1957;
54:377-411
1287
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1288
Mador MJ, Kufel TJ. Reproducibility of visual analog scale measurements of dyspnea in patients with chronic
obstructive pulmonary disease. Am Rev Respir Dis 1992; 146:82-87
1289
Noseda A, Carpiaux JP, Schermber J, Yernault JC. Dyspnoea assessed by visual analogue scale in patients with
chronic obstructive lung disease during progressive and high intensity exercise. Thorax 1992; 47:363-368
1290
Abernethy AP, Currow DC, Frith P, Fazekas BS, et al. Randomised, double blind, placebo controlled crossover
trial of sustained release morphine for the management of refractory dyspnoea. Br Med J 2003; 327:523-528
1291
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1278
154
Baseline Dyspnoea Index (BDI) / Transition Dyspnoea Index (TDI)
The BDI is a complex questionnaire divided into three components1292. These address the degree of
“functional impairment” (relating to disability due to breathlessness), magnitude of the task required to
produce the breathlessness, and the magnitude of the effort that produces shortness of breath. Each
component is divided into five grades. It was proposed that each of the three components contributed
different elements to the sensation of dyspnoea1293.
A trained observer asking open-ended questions about symptoms administers the BDI, and then scores
each category in turn by interpreting the patient’s responses as a degree of impairment related to dyspnoea
for each component. The three ratings (each between 0 and 4) are added to create a “focal score” (0 to 12,
with 12 indicating no impairment, and 0 indicating the most severe disability possible). Questioning by
experienced observers is takes between 2 and 5 minutes1294,1295. BDI has been extensively validated in a
variety of respiratory diseases including COPD, and its reliability and validity are high1296,1297. BDI
correlates with severity of airways obstruction (r with FEV1 =0.31 to 0.42)1298,1299, inspiratory muscle
strength (r with Pimax=0.43 to 0.49)1300,1301, and maximum oxygen uptake (r with VO2max =0.46), but not
with degree of gas trapping (r= -0.14) 1302. Good correlations have been shown between BDI and physical
functioning, role functioning, health perceptions and social functioning dimensions of the Medical
Outcomes Scale (MOS) Short Form (SF) 20-item instrument of generic HRQoL (r=0.36 to 0.70)1303, MRC
Dyspnoea Scale (r=0.61 to 0.70)1304, and Oxygen Cost Diagram (r=0.48-0.54)1305.
The Transition Dyspnoea Index (TDI) includes the same three components as the BDI, but the questions
posed now relate to a rating of the degree of change from the previous score, ranging from –3 (very
marked deterioration), through 0 (no change), to +3 (the greatest possible improvement)1306. In the TDI a
score change by 1 or more represents clinically meaningful change, and such changes have been shown to
have good face validity (eg in a long-term tiotropium trial1307). In a prospective uncontrolled study
comparing the responsiveness of a range of outcome measures to PR, a clinically significant change in TDI
was found in over 50% of patients, with similar percentages showing meaningful changes in VAS at peak
1292
Mahler DA, Weinberg DH, Wells CK, Feinstein AR. The measurement of dyspnoea: contents, interobserver
agreement, and physiologic correlates of two new clinical indexes. Chest 1984; 85:751-758
1293
Stoller JK, Ferranti R, Feinstein AR. Further specifications of a new clinical index for dyspnoea. Am Rev Respir
Dis 1986; 134:1129-1134
1294
Stoller JK, Ferranti R, Feinstein AR. Further specifications of a new clinical index for dyspnoea. Am Rev Respir
Dis 1986; 134:1129-1134
1295
Mahler DA, Faryniarz K, Tomlinson D, Colice GL, et al. Impact of dyspnea and physiologic function on general
health status in patients with chronic obstructive pulmonary disease. Chest 1992; 102:395-401
1296
Mahler DA, Faryniarz K, Tomlinson D, Colice GL, et al. Impact of dyspnea and physiologic function on general
health status in patients with chronic obstructive pulmonary disease. Chest 1992; 102:395-401
1297
Mahler DA, Rosiello RA, Harver A, Lentine T, et al. Comparison of clinical dyspnoea ratings and psychophysical
measurements of respiratory sensation in obstructive airway disease. Am Rev Respir Dis 1987; 135:1229-1233
1298
Mahler DA, Faryniarz K, Tomlinson D, Colice GL, et al. Impact of dyspnea and physiologic function on general
health status in patients with chronic obstructive pulmonary disease. Chest 1992; 102:395-401
1299
Mahler DA, Rosiello RA, Harver A, Lentine T, et al. Comparison of clinical dyspnoea ratings and psychophysical
measurements of respiratory sensation in obstructive airway disease. Am Rev Respir Dis 1987; 135:1229-1233
1300
Stoller JK, Ferranti R, Feinstein AR. Further specifications of a new clinical index for dyspnoea. Am Rev Respir
Dis 1986; 134:1129-1134
1301
Hajiro T, Nishimura K, Tsukino M, Ikeda A, et al. Analysis of clinical methods used to evaluate dyspnoea in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 158:1185-1189
1302
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1303
Hajiro T, Nishimura K, Tsukino M, Ikeda A, et al. Analysis of clinical methods used to evaluate dyspnoea in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 158:1185-1189
1304
Mahler DA, Wells CK. Evaluation of clinical methods for rating dyspnea. Chest 1988; 93:580-586
1305
Lareau SC, Meek PM, Press D, et al. Dyspnea in patients with chronic obstructive pulmonary disease: Does
dyspnea worsen longitudinally in the presence of declining lung function? Heart Lung 1999; 28:65-73
1306
Mahler DA, Faryniarz K, Tomlinson D, Colice GL, et al. Impact of dyspnea and physiologic function on general
health status in patients with chronic obstructive pulmonary disease. Chest 1992; 102:395-401
1307
Witek TJ, Mahler DA. Minimal important difference of the transition dyspnoea in a multinational clinical trial.
Eur Respir J 2003; 21:267-272
155
exercise and in CRDQ1308. The most significant changes seen were in BDI/TDI magnitude of task score
(p<0.0001), and the change in BDI/TDI was most closely correlated with change in CRDQ Mastery Score
(r=0.65) and change in MRC Score (r=0.37)1309.
Interpretation of Breathing Problems Questionnaire (IBPQ)
This self-report questionnaire was designed to evaluate the impact of dyspnoea on people with COPD in
terms of catastrophising thoughts1310. A short version (IBPQ-S) has been found to have good psychometric
properties (internal consistency, Cronbach’s α=0.87; inter-rater reliability, κ=0.63; test-retest reliability
Wilcoxon matched pairs signed rank test p<0.05), and related to anxiety triggered by dyspnoea in a
comparison with HADS (r=0.79) in 30 patients with severe COPD1311.
When these issues related to panic need to be considered, this instrument looks to provide reliable insight.
Pulmonary Functional Status and Dyspnoea Questionnaire (PFSDQ)
This measure was developed and partly validated to measure both the level of dyspnoea with activities and
changes in functional ability1312. It contains 164 items presenting 79 activities of daily living that the
patient nominates. The patient nominates the intensity of dyspnoea associated with the activities, as well as
any alteration in their functional ability to perform each activity as a result of their COPD. The activities
presented are relevant for adults of either gender, reflecting a range of energy requirements, grouped into
scales of self care, mobility, eating, home management, social and recreational. Validation shows good
validity, stability and reliability for both the dyspnoea and the functional ability domains1313. Changes in
dyspnoea do not appear to match declines in lung function over time. Dyspnoea with activities requiring
arm elevation showed the sole relationship with rate of FEV1 decline over time.
This tool appears to be useful in research, though no data on its responsiveness to change following
interventions have been published. It appears complex and time-consuming and unsuited to routine clinical
practice as either an initial assessment or an outcome measure for PR.
Dyspnoea Management Questionnaire (DMQ-30)
This instrument was designed to enumerate the behavioural impact of breathing distress and a person’s
perceived ability to cope with the dyspnoea1314. It has 30 items that address five dimensions – intensity of
dyspnoea, anxiety related to dyspnoea, fearful anxiety avoidance, self-efficacy for activity, and satisfaction
with strategy usage. Each question has a 7-point Likert scale. High levels of internal consistency
(Cronbach’s α = 0.87-0.96) and test-retest reliability (intraclass correlation coefficient = 0.71-0.95) have
been shown in 85 COPD patients (mainly female). Relevant items correlated well with SOLQ, SF-12 and
HADS (see below). Responsiveness to therapeutic interventions and correlations with disease severity as
well as other elements of validation still need to be completed, but this instrument looks to have promise as
an indicator of the symptom of dyspnoea and its impact at the very least.
1308
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1309
Lareau SC, Meek PM, Press D, et al. Dyspnea in patients with chronic obstructive pulmonary disease: Does
dyspnea worsen longitudinally in the presence of declining lung function? Heart Lung 1999; 28:65-73
1310
Sutton K, Cooper M, Pimm J, Wallace L. Anxiety in chronic obstructive pulmonary disease: the role of illness
specific catastrophic thoughts. Cognitive Therapy Res 1999; 25:573-585
1311
Gurney-Smith B, Cooper M, Wallace L. Anxiety and panic in chronic obstructive pulmonary disease: the role of
catastrophic thoughts. Cognitive Therapy Res 2002; 26:143-155
1312
Lareau SC, Meek PM, Roos PJ. Development and testing of the modified version of the Pulmonary Functional
Status and Dyspnea Questionnaire (PFSDQ-M). Heart Lung 1998; 27:159-168
1313
Lareau SC, Meek PM, Press D, et al. Dyspnea in patients with chronic obstructive pulmonary disease: Does
dyspnea worsen longitudinally in the presence of declining lung function? Heart Lung 1999; 28:65-73
1314
Norweg AM, Whiteson J, Demetis S, Rey M. A new functional status measure of dyspnoea and anxiety for adults
with lung disease: the Dyspnoea Management Questionnaire. J Cardiopulm Rehabil 2006; 26:395-404
156
UCSD Shortness of Breath Questionnaire (SOBQ)
This tool was developed in University of California San Diego, and has been used extensively in one of the
foremost PR programs in USA, revised and validated. It appears suited to research if not clinical care1315. It
includes 21 activities of daily living covering a range of energy expenditures, and asks patients to rate the
severity of dyspnoea they estimate they would experience on a 6-point scale. Three additional questions
seek how much limitation there is in their everyday life from (i) shortness of breath, (ii) fear of hurting
oneself by over-exerting, and (iii) fear of shortness of breath. Cross-sectional comparisons with FEV1,
FVC, DLCO, QWB, CES-D, 6MWD, and perceived dyspnoea at the end of a 6MWT showed interesting
correlations. Overall health status (QWB) and level of depression (CES-D) correlated significantly, as did
most physiological measures, 6-MWD (r= -0.68) and Borg dyspnoea (r= +0.45). The authors suggest the
SOBQ is a reliable and valid measure of dyspnoea, ideally suited to research applications. In a large
randomised trial comparing comprehensive PR with an education-alone intervention SOBQ improved in
both groups, but significantly more in the comprehensive PR group1316, confirming the responsiveness of
the measure. In this same study SOBQ was significantly associated with survival.
The SOBQ has been evaluated for responsiveness alongside other measures, in 164 patients with COPD
attending PR. The minimum clinically important difference (MCID) for SOBQ in this study was five units
(compared to 0.47 for the CRDQ – in line with previous studies with this instrument – and 0.031 for QWB
– also similar to reported levels of significance)1317.
Other measures
HRQoL measures like the CRDQ and SGRQ (described below) can describe the impact of breathlessness
on health status. It has been suggested that measures of dyspnoea found in these comprehensive diseasespecific health status assessments, notably the Activity dimension of the SGRQ and Dyspnoea component
of the CRDQ, may be as useful as the MRC Scale or the BDI1318. In that study, these measures seemed
closely inter-related, but there was a distinct difference between Borg at Maximal exercise and other
dyspnoea indicators. This difference may relate to the fact that the Borg was measured at maximal
exertion, while the impact of dyspnoea on activities required the patient recall their experiences remotely
from the activities.
5.2 Measures of Impairment
Physiological Impairments
Asthma and COPD are characterised by airflow limitation. In asthma there is variability in symptoms and
reversibility of airflow limitation following bronchodilator administration, while in COPD the symptoms
are more consistent from day to day and bronchodilator responsiveness is incomplete. The measurement of
airflow limitation is imperative in all people with respiratory symptoms - as a diagnostic tool, an indicator
as severity, and a prognostic indicator.
Spirometry
The most robust test of respiratory impairment is spirometry, from which a large number of variables can
be derived. Spirometry requires certain fundamental actions. These include use of a reliable and
appropriately calibrated device, adequately trained staff, and assurance of full effort by the patient.
1315
Eakin EG, Resnikoff PM, Prewitt LM, et al. Validation of a new dyspnoea measure. The UCSD Shortness of
Breath Questionnaire. Chest 1998; 113:629-634
1316
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995; 122:823-832
1317
Kupferberg DH, Kaplan RM, Slymen DJ, Ries AL. Minimal clinically important difference for the UCSD
shortness of breath questionnaire. J Cardiopulm Rehabil 2005; 25:370-377
1318
Bestall JC, Paul EA, Garrod R, Garnham R, et al. Usefulness of the Medical Research Council (MRC) dyspnoea
scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 1999; 54:581-586
157
For a reliable measurement, the patient must inhale fully to total lung capacity (TLC) then, with lips
completely sealed around the mouthpiece, as rapidly and as completely as possible forcibly exhale to
residual volume (RV). Efforts should be repeated at standard intervals to ensure consistency of results, and
the best effort is taken as the reported measurement. To evaluate bronchodilator reversibility a standard
dose of a bronchodilator is administered, with every effort again to ensure optimal inhalation of the dose
by the patient. The spirometry test is repeated twenty minutes later. Again the best effort test is used as the
reported measurement, and the change from the pre-bronchodilator result is calculated, and then divided by
the predicted value to obtain the percent bronchodilator response1319.
Results quote the FEV1 and the FVC, and their change after bronchodilator, as well as the ratio of
FEV1/FVC1320,1321. Predictions based on race, gender, age and height are used as reference points. Since
FEV1 and VC are reproducible over a long period (Coefficient of Variation, CV <10%)1322, they can be
considered reliable measures in diagnosis, severity rating and response to treatment. That is, they are
applicable as clinical indicators and outcome measures. There are several useful checkpoints:
• An FEV1/FVC ratio below 0.70 in adults or below 0.80 in children indicates the presence of
airflow limitation.
• In such cases, the level of FEV1 in relation to predicted values is a guide to the grade of severity of
the airflow limitation.
• Improvement in FEV1 and/or FVC by more than 15% and by more than 0.30 litres after
bronchodilator is considered a significant bronchodilator response, suggestive of asthma if clinical
features are also present.
• An FEV1/FVC ratio above 0.75 in adults with individual values of FEV1 and / or FVC below 80%
predicted suggests the presence of a restrictive disorder. Such findings can also be seen, however,
when airflow limitation results in dynamic airway compression and gas trapping. In such cases it is
advisable to measure TLC and its subdivisions.
Other measures are also available from the forced expiratory test, especially if the data are electronically
derived. Expiratory flow rates at specific lung volumes (eg MEF50), or average flow rate over the middle
half of the expiration (eg FEF 25-75 or MMEF), are sometimes used as guides to the presence of early or
very mild airflow limitation, especially in small airways. Such measurements are more variable (have
wider confidence intervals), and are therefore less robust than the highly repeatable FEV1. The appearance
of the expiratory flow-volume curve (Diagram 1) gives an appreciation of the effects of airflow limitation,
with reduced peak expiratory airflow in severe cases, a concave expiratory limb, and shifting of the
operating lung volumes with gas trapping and hyperinflation.
1319
Pierce RJ, Hillman D, Young IH, et al. Respiratory function tests and their application. Respirology 2005; 10:S1-
S19
1320
Quanjer PH, Tammerling GJ, Cotes JE, Pedersen OF, et al. Lung volumes and forced ventilatory flows. Report
Working Party, Standardization of lung function tests. European Community for Steel and Coal. Eur Respir J 1993; 6
(Suppl 16):5-40
1321
Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories (Crapo RO, Chairman).
Standardization of spirometry; 1994 update. Am J Respir Crit Care Med 1995; 152:1107-1136
1322
Noseda A, Carpiaux JP, Prigogine T, Schmerber J. Lung function, maximum and submaximum exercise testing in
COPD patients: reproducibility over a long interval. Lung 1989; 167:247-257
158
FIGURE 5.1.
SPIROMETRY (VOLUME-TIME PLOT) IN NORMAL PATIENT AND COPD PATIENT
FIGURE 5.2.
TYPICAL FLOW-VOLUME CURVES IN NORMAL AND COPD PATIENTS
MONITORING LUNG DISEASE
KEY POINT
Managing respiratory disease without spirometry and disability
measures is similar to diagnosing and treating hypertension
diabetes without measuring blood pressure or blood glucose or the
impacts of these diseases on the individual.
159
TABLE 5.2.
FEV1 USES AS A CLINICAL INDICATOR AND OUTCOME MEASURE
Rationale for FEV1
Usefulness of FEV1
Diagnosis1323,1324
FEV1/FVC <0.70 indicates airflow limitation
FEV1 improvement post-bronchodilator > 12% above predicted suggests asthma
FEV1 fall > 20% post-bronchoconstrictor (e.g. histamine, methacholine, standard
exercise) indicates airway hyper-responsiveness, a critical property of asthma
Level of FEV1 is an indicator of severity of airflow limitation in asthma and COPD
Level of FEV1 is used by GOLD to define severity grading for COPD
FEV1 predicts all-cause mortality in a general population
FEV1 predicts outcome from hospital care of COPD exacerbation
Annual rate of decline in FEV1 predicts survival in COPD
Annual rate of decline in FEV1 slows after smoking cessation
Test of reversibility with beta-agonist in asthma
Indicator of reversibility with inhaled corticosteroids in asthma
Small responses to bronchodilators may occur in COPD
Response to inhaled corticosteroids in COPD is usually small
There is minimal response in FEV1 to pulmonary rehabilitation despite
improvements in disability measures
Severity rating1325
Prognostic
indicator1326,1327,1328,1329
Outcome
measure1330,1331,1332
Complex Lung Function
Other testing procedures are used to derive static FRC, TLC and other subdivisions of lung volume, gas
1333,1334,1335,1336.
transfer of carbon monoxide, and a range of other functions (see Introduction)
These can
help understand the effects of airflow limitation (such as gas trapping and hyperinflation) and the
efficiency of gas exchange. While they can help to categorise the patient’s physiology and disease severity,
they are not useful outcome measures, as they remain essentially unchanged after PR, even when high
1323
Quanjer PH, Tammerling GJ, Cotes JE, Pedersen OF, et al. Lung volumes and forced ventilatory flows. Report
Working Party, Standardization of lung function tests. European Community for Steel and Coal. Eur Respir J 1993; 6
(Suppl 16):5-40
1324
Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories (Crapo RO, Chairman).
Standardization of spirometry; 1994 update. Am J Respir Crit Care Med 1995; 152:1107-1136
1325
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease.
Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report. National Institutes of
Health; NHLBI Publication Number 2701. April 2001
1326
Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J 1977; 1:1645-1648
1327
Traver GA, Cline MG, Burrows B. Predictors of mortality in chronic obstructive pulmonary disease. A 15-year
follow-up study. Am Rev Respir Dis
1328
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995; 122:823-832
1329
Anthonisen NR, Connett JE, Kiley JP, Altose MD, et al. Effects of smoking intervention and the use of an inhaled
anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA 1994; 272:1497-1505
1330
Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories (Crapo RO, Chairman).
Standardization of spirometry; 1994 update. Am J Respir Crit Care Med 1995; 152:1107-1136
1331
Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease.
Global Initiative for Chronic Obstructive Lung Disease. NHLBI/WHO Workshop Report. National Institutes of
Health; NHLBI Publication Number 2701. April 2001
1332
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995; 122:823-832
1333
Quanjer PH, Tammerling GJ, Cotes JE, Pedersen OF, et al. Lung volumes and forced ventilatory flows. Report
Working Party, Standardization of lung function tests. European Community for Steel and Coal. Eur Respir J 1993; 6
(Suppl 16):5-40
1334
Committee on Proficiency Standards for Clinical Pulmonary Function Laboratories (Crapo RO, Chairman).
Standardization of spirometry; 1994 update. Am J Respir Crit Care Med 1995; 152:1107-1136
1335
Stocks J, Quanjer PH. Reference values for residual volume, functional residual capacity and total lung capacity.
ATS Workshop on Lung Volume Measurements. Eur Respir J 1995; 8:492-506
1336
Cotes JE, Chinn DJ, Quanjer PH, Roca J, Yernault J-C. Standardization of the measurement of transfer factor
(diffusing capacity). Report Working Party. Standardization of lung function tests. European Community for Steel
and Coal. Eur Respir J 1993; 6 (Suppl 16):41-52
160
levels of exercise re-training are included1337,1338. They often do change, on the other hand, after surgical
interventions.
Arterial Blood Gas Measurements
Blood gas measurements are also performed on blood taken from an artery (usually brachial or radial) to
determine the adequacy of oxygenation, gas exchange efficiency, adequacy of ventilation, and acid-base
status. These tests do not change after comprehensive PR or any of its components (including exercise
training).
Tests of Static Physiological Impairment
Key Points
Spirometry remains the simplest, most reliable and clinically useful of all
physiological tests.
In respiratory disease spirometry is an essential tool for diagnosing airflow
limitation, assessing bronchodilator responsiveness, and classifying clinical
severity.
Knowledge of arterial blood gases is also vital, as both oxygenation and
ventilation (through pCO2) can be assessed.
Gas transfer is reduced in the presence of emphysema but not in asthma and
this can add to diagnostic specificity.
Lung volume measurements reflect the effects of airflow limitation (distal gas
trapping and static hyperinflation).
Spirometry, gas transfer and arterial blood gas analysis are not useful outcome
measures in PR because they do not change post-PR, although reduced
hyperinflation can occur.
Exercise impairment
(a)
Maximal exercise testing
Maximal (symptom-limited) tests can provide measurement of peak oxygen uptake and a range of other
indicators of exercise impairment1339.
Incremental Exercise Tests
ERGOMETER TESTING
These tests require a carefully calibrated treadmill or cycle ergometer, fast response gas analysers,
electrocardiograph, pulse oximeter, and a device to monitor airflow at the mouth. The equipment is
1337
Nici L, Donner C, Wouters E, ZuWallack R, et al, on behalf of the ATS/ERS Pulmonary Rehabilitation Writing
Committee. American Thoracic Society/European Respiratory Society Statement on Pulmonary Rehabilitation. Am J
Respir Crit Care Med 2006; 173:1390-1413
1338
British Thoracic Society Standards of Care Subcommittee on Pulmonary Rehabilitation. Pulmonary rehabilitation.
Thorax 2001; 56:827-834
1339
ERS Task Force on Standardization of Clinical Exercise Testing. Clinical exercise testing with reference to lung
disease. Indications, Standardization, and interpretation strategies. Eur Respir J 1997; 10:1662-1689
161
expensive, the tests are time-consuming for setting-up, conducting and interpreting. Patients often dislike
incremental maximal exercise tests because they demand maximal effort and often produce distressing
symptoms. However, for accuracy and variety of information about training effects, they are the gold
standard. In addition to the physiologic measures it is useful to ask the patient at regular intervals to elect a
rating of perceived exertion, breathing difficulty and leg fatigue, using modified Borg scales.
The best form of ergometry is debated. Cycle ergometry is generally considered to provide more reliable
results, for several reasons. Quantitation of work performed on a treadmill depends on body weight,
stepping cadence, use of arms or shoulder girdle by gripping handrails, and posture (e.g. stooping) can all
affect metabolic requirements, and therefore the correlation between apparent level of exercise and actual
work performed. Cycle ergometry equipment is cheaper, less space occupying and less noisy. There is
greater body stability on the cycle, so ventilation, pulse oximetry and ECG measurements are more stable.
For rare patients, however, cycling is impossible and a treadmill is useful. Non-invasive incremental
symptom-limited maximal ergometry testing derives the variables shown in Table 5.3. The two parameters
derived from exercise testing with least variability over time (CV <10%) in patients with COPD are VE
max and VO2 max1340 making them useful outcome measures for treatment interventions.
FIGURE 5.3
CYCLE ERGOMETRY IS HELPFUL IN DETERMINING MAXIMUM EXERCISE CAPACITY AND
CLARIFYING CAUSES OF DYSPNOEA
An important contribution to the understanding of the cause of dyspnoea is dynamic hyperinflation. In
people without airflow limitation, there are large reserves in expiratory and inspiratory flows that allow
increased ventilation to be achieved without altering operating lung volumes (i.e. higher tidal volume is
achieved by increasing flow at iso-volume, reducing tidal end-expiratory volume and increasing tidal endinspiratory volume). In people with airflow limitation, however, a limit to the expiratory flow and
sometimes to inspiratory flow during tidal breathing, either at rest or during exertion, is imposed by airway
geometry and lung/airway elastic recoil, and it becomes increasingly difficult to empty the lungs. Increased
ventilation can only be achieved by a progressive increase in tidal end-expiratory lung volume, forcing the
tidal end-inspiratory volume even higher. In more severe COPD, the static overinflation due to loss of lung
elastic recoil with emphysema worsens the dynamic hyperinflation of exercise1341. By measuring
inspiratory capacity (IC) before and during exercise it is possible to observe this dynamic
1340
Noseda A, Carpiaux JP, Prigogine T, Schmerber J. Lung function, maximum and submaximum exercise testing in
COPD patients: reproducibility over a long interval. Lung 1989; 167:247-257
1341
Ferguson G. The ins and outs of breathing: an overview of lung mechanics. Eur Respir Rev 2004; 13:30-34
162
hyperinflation1342. Dynamic hyperinflation results in higher work of breathing, as much greater inspiratory
pressures are required to overcome the higher elastic recoil for a given change in lung volume1343. This
increased work of breathing relates closely to breathlessness1344,1345.
Several different types of training effects occur after exercise training programs in COPD. The magnitude
of these effects is determined by the type and intensity of the exercise undertaken and the duration of the
program. For example, strength is built by strength training and endurance training increases endurance in
athletes1346, and this probably applies to people with COPD1347. Moreover, the training effects from
exercise training are specific to the muscle group exercised1348. In spite of these apparent limitations, other
benefits from training have been observed in maximal exercise testing of people with COPD, albeit with
some inconsistencies. These include increased work capacity1349 and peak oxygen uptake1350,1351, improved
ventilatory function1352, reduced lactate production1353 and reduced heart rate response1354. Functional
effects perceived by the patient include extended exercise endurance1355, better self-efficacy for
exercise1356, less perceived dyspnoea with exertion1357, reduced dependence1358, less depression1359, and
better HRQoL1360.
1342
O’Donnell DE, Revill SM, Webb KA. Dynamic hyperinflation and exercise intolerance in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 2001; 164:770-777
1343
O’Donnell DE, Revill SM, Webb KA. Dynamic hyperinflation and exercise intolerance in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 2001; 164:770-777
1344
O’Donnell DE, Lam M, Webb KA. Measurement of symptoms, lung hyperinflation, and endurance during
exercise in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 158:1557-1565
1345
Aliverti A, Stevenson N, Dallaca RL, et al. Regional chest wall volumes during exercise in chronic obstructive
pulmonary disease. Thorax 2004; 59:210-216
1346
Maughan R, Gleeson M, Greenhaff PL. Biochemistry of exercise and training. Oxford: Oxford University Press
1997
1347
Simpson K, Killian K, McCartney N, Stubbing DG, Jones NL. Randomized controlled trial of weightlifting
exercise in patients with chronic airflow limitation. Thorax 1992; 47:70-75
1348
Lake FR, Henderson K, Briffa T, Openshaw J, Musk AW. Upper-limb and lower-limb exercise training in
patients with chronic airflow obstruction. Chest 1990; 97:1077-1082
1349
Punzal PA, Ries AL, Kaplan RM, Prewitt LM. Maximum intensity exercise training in patients with chronic
obstructive pulmonary disease. Chest 1991; 100:618-623
1350
Wijkstra PJ, Van Altena R, Kraan J, et al. Quality of life in patients with chronic obstructive pulmonary disease
improves after rehabilitation at home. Eur Respir J 1994; 7:269-273
1351
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995; 122:823-832
1352
Bass H, Whitcomb JF, Forman R. Exercise training: therapy for patients with chronic obstructive pulmonary
disease. Chest 1970; 57:116-121
1353
Casaburi R, Wasserman K, Patession A, Ioli F, et al. A new perspective in pulmonary rehabilitation: anaerobic
threshold as a discriminant in training. Eur Respir J 1989; 2( Suppl 7):618s-623s
1354
Bass H, Whitcomb JF, Forman R. Exercise training: therapy for patients with chronic obstructive pulmonary
disease. Chest 1970; 57:116-121
1355
Chester EH, Belman MJ, Bahler RC, et al. Multidisciplinary treatment of chronic pulmonary insufficiency: 3. The
effects of physical training on cardiopulmonary performance in patients with chronic obstructive pulmonary disease.
Chest 1977 72:695-702
1356
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995; 122:823-832
1357
Reardon J, Awad E, Normandin E, Vale F, et al. The effect of comprehensive outpatient pulmonary rehabilitation
on dyspnoea. Chest 1994; 105:1046-1052
1358
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at 1 year of outpatients multidisciplinary
pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
1359
Cambach W, Wagenaar RC, Koelman TW, et al. The long-term effects of pulmonary rehabilitation in patients
with asthma and chronic obstructive pulmonary disease: a research synthesis. Arch Phys Med Rehab 1999; 80:103111
1360
Lacasse Y, Brosseau L, Milne S, Martin S, et al. Pulmonary rehabilitation for chronic obstructive pulmonary
disease. Cochrane Database of Systematic Reviews 2002; Issue 3
163
TABLE 5.3. MEASUREMENTS DERIVED FROM MAXIMAL INCREMENTAL EXERCISE TESTING
Measure
Abbrev
-iation
Definition
Use/Interpretation
Maximum work rate
W max
Heart rate at
maximum work
Ventilation at
maximum work
HR max
Maximum voluntary
ventilation
MVV
Maximum effort possible.
Predicted relates to age, gender, weight
Limit of HR response.
Predicted relates to age
Non-limiting in normal, except in elite
athletes. May be limiting in respiratory
diseases. Breathing reserve at Wmax is
usually >25%.
Reduced in respiratory and chest wall
disorders
Breathing Reserve
BR
Work rate (watts) achieved at
maximal effort
Highest heart rate (beats per min),
usually at maximum effort
Highest ventilation achieved (L per
min), usually at maximum effort.
Can be compared to maximum
voluntary ventilation
Upper limit of the body’s ability to
ventilate the lungs (measured from
12 seconds effort, or calculated
from FEV1)
Gap between VEmax and MVV
Maximum oxygen
uptake
VO2 max
Highest oxygen uptake (L per min)
obtainable despite increasing effort
and work. Peak VO2 may be lower
than VO2max
Oxygen pulse
VO2/HR
Amount of O2 extracted by body
tissues in each cardiac stroke
volume
Anaerobic threshold
(AT)
VO2 AT
Oxygen uptake-Work
rate relationship
О”VO2/О”H
R
Exercise VO2 above which
anaerobic energy production
significantly supplements aerobic,
with increasing lactic acidosis and
accelerated increase in ventilation
How much O2 is utilised by the
body for a given level of external
work – the coupling of external to
cellular respiration
Carbon dioxide
output
Ventilatory
equivalent for CO2
VCO2
Ventilatory
equivalent for O2
VE/VO2
Ratio of VE and VO2.
Reflects ventilation and perfusion
matching
Oxygen saturation
SpO2
Arterial oxygen saturation
measured with a pulse oximeter
probe on earlobe or finger-tip
VE max
VE/VCO2
Output of CO2 from metabolism (L
per min) exhaled from the body
Ratio of VE and VCO2.
Index of dead space ventilation
High when exercise limited by cardiac &
vascular disorders or poor effort.
Low with lung disorders
Predicted relates to age, gender, height,
weight, activity levels.
Determined by cardiac output, muscle O2
extraction potential, and ventilation
capacity.
Reflects maximal cardiac output
Determined by stroke volume and arteriovenous O2 content difference.
High in fit and beta-blocked patients.
Low in cardiac pump disorders
Normally <40% pred VO2max.
Low in peripheral vascular, cardiac,
pulmonary vascular, respiratory and
anaemic disorders
Obese need more VO2 per unit of work.
Reduced slope if reduced O2 delivery
(e.g. cardiovascular or mitochondrial).
Increased if anaerobic metabolism or high
VO2 by breathing muscles
Increased with hyper-metabolic states
(e.g. hyperthyroid, obesity)
Declines till ventilatory compensation
after AT then increases.
Increased (>32) with high dead space
(pulmonary vascular, right-left shunt,
ventilatory impairment, hyperventilation)
Declines till AT then increases.
Increased (>28) with high dead space and
hyperventilation.
Low with chemoreceptor insensitivity
Usually above 95%.
Significant hypoxaemia may occur with
small decrement in SpO2.
Significant change = 4%; severe
desaturation <88%
164
THE INCREMENTAL SHUTTLE WALK TEST (ISWT)
The ISWT has been more recently developed1361 and validated in COPD and heart failure1362 as a more
tolerable test of impairment that requires little in the way of equipment. It correlates with VO2max from
incremental ergometry1363. This test has been criticized that it does not reflect normal daily activities
(unlike submaximal walking tests – see below), but it is responsive to treatment with medications1364 and
physical treatments including pulmonary rehabilitation.
The ISWT is walked over a 10-metre "there-and back" circuit, Patients are instructed and guided by
cassette tape or compact disc recording to walk at fixed pace so they reach the end of each 10-metre lap at
the same time as a “beep”. The pace is incremented every minute by 0.17m/sec through 12 increments of
speed (“levels”). The test is symptom-limited, and the end of test is judged if the patients does not
complete the distance (“lap”) in the required time or is too breathless to continue.
FIGURE 5.5
INCREMENTAL SHUTTLE WALK TEST OVER A 10-METRE COURSE
1361
Singh SJ, Morgan MDL, Scott S, et al. Development of a shuttle walking test of disability in patients with chronic
airways obstruction. Thorax 1992; 47:1019-1024
1362
Gree DJ, Watts K, Rankin S, et al. A comparison of the shuttle and 6 minute walking tests with measured peak
oxygen consumption in patients with heart failure. J Sci Med Sport 2001; 4:292-300
1363
Singh SJ, Morgan MDL, Hardman AE, et al. Comparison of oxygen uptake during a conventional treadmill test
and shuttle walking test in chronic airflow limitation. Eur Respir J 1994; 7:2016-2020
1364
Brightling CE, Monteiro W, Ward R, Parker D, et al. Sputum eosinophilia and short-term response to
prednisolone in chronic obstructive pulmonary disease: a randomised controlled trial. Lancet 2000; 356:1480-1485
165
(b)
Submaximal Exercise Tests
These tests are generally considered more indicative of disability (see also below). They are usually more
closely related to a person's ability to conduct normal activities such as walking, being largely self-paced
endurance tests. They are useful for comparing changes over time (e.g. following treatment intervention).
THE SIX-MINUTE WALK TEST (6MWT)
This was derived from a 12-minute walk test1365,and is conducted in a corridor around 40 to 50 metres
long1366. Patients are instructed to walk at their own pace, though as briskly as they can manage, and to
cover as much distance as possible in the time allocated. Usually a pulse oximeter is worn. While the
patient is encouraged to persist, rests are allowed for severe breathlessness, leg pain, chest pain, severe
fatigue, or severe oxygen desaturation. In addition the patient can be asked to rate the perceived
breathlessness and effort using Borg scores.
There has been substantial validation of the 6-minute walk test in different patient populations examining a
variety of potential influencing factors. Details of these can be found in a systematic review1367. Reference
equations have been developed for healthy individuals at various ages1368,1369,1370, and these have been
compared and validated ina population of 1,379 COPD patients1371. In this study a 6MWD value below 350
metres indicated a worse prognosis, especially in females. The same workers had earlier found that 6MWD
appeared at least as good as a prognostic indicator as peak oxygen uptake (VO2max) in people with
COPD1372.
The systematic review also established that the minimum clinically significant change in six-minute walk
distance (6MWD), based on its intra-individual repeatability, is 49 metres, although further reliable
analysis suggests 54 metres represents the minimum clinically important difference (MCID)1373.
Improvements in 6MWD correlate with changes in dyspnoea ratings after therapeutic interventions1374. The
6MWT has been compared with the ISWT and cycle ergometry1375. This study indicates that in the selfpaced 6MWT, when the protocol is properly applied, equivalent heart rates and levels of dyspnoea were
achieved. Heart increments, however, were linear in the ISWT and ergometry and alinear in the 6MWT,
while the dyspnoea increases were linear with time in the 6MWT and alinear in the ISWT and ergometry.
1365
McGavin CR, Gupta SR, McHardy GJR. Twelve-minute walking test for assessing disability in chronic
bronchitis. Br Med J 1976; 1:822-823
1366
Carter R, Holliday DB, Nwasurba C, Stocks J, et al. 6-minute walk work for assessment of functional capacity in
patients with COPD. Chest 2003; 123:1408-1415
1367
Solway S, Brooks D, Lacasse Y, Thomas S. A qualitative systematic overview of the measurement properties of
functional walk tests used in the cardiorespiratory domain. Chest 2001; 119:256-270
1368
Enright PL, Sherrill DL. Refernce equations for the six-minute walk in healthy adults. Am J Respir Crit Care Med
1998; 158:1384-1387
1369
Troosters T, Gosselink R, Decramer M. Six minute walking distance in healthy elderly subjects. Eur Respir J
1999; 14:270-274
1370
Carter R, Holiday D, Nwasurba C, Stocks J, Grothues C, Tiep B. 6-minute walk work for assessment of
functional capacity in patients with COPD. Chest 2003; 123:1408-1415
1371
Cote CG, Casanova C, Marin JM, Lopez MV, Pinto-Plata V, et al. Validation and comparison of reference
equations for the 6-min walk distance test. Eur Respir J 2008; 31:571-578
1372
Cote CG, Pinto-Plata V, Kasprzyk K, Dordelly LJ, Celli BR. The 6-min walk distance, peak oxygen uptake, and
mortality in COPD. Chest 2007; 132:1778-1785
1373
Enright PL, McBurnie MA, Bittner V, Tracy RP, et al. The 6-min walk test. A quick measure of the functional
status of elderly adults. Chest 2003; 123:387-397
1374
Niederman MS, Clemente PH, Fein AM, Feinsilver SH, et al. Benefits of a multidisciplinary pulmonary
rehabilitation program: improvements are independent of lung function Chest 1991; 99:798-804
1375
Turner SE, Eastwood PR, Cecins NM, et al. Physiologic responses to incremental and self-paced exercise in
COPD. A comparison of three tests. Chest 2004; 126:766-773
166
The 6MWD is an independent predictor of mortality in people with COPD1376, and it has been included in
a composite prognostic rating of COPD, known as the BODE Index1377.
ENDURANCE SHUTTLE WALK TEST (ESWT)
This test has been carefully validated to determine change from interval to interval1378. It utilizes the same
10-metere course and auditory signals as the ISWT, but the pace is fixed (at 75% to 85% of the maximum
level or speed reached in a prior ISWT), and the patient is cued to complete as many laps as symptoms
allow (i.e. �until they can go no further’). Revill also recommends a time limit of 20 minutes, though the
patient is not made aware of this limit. A pulse oximeter can be used to monitor oxygen saturation
throughout, and Borg ratings can be obtained, as in the 6MW.
The ESWT has been shown to be responsive to rehabilitation1379, to bronchodilators used in
COPD1380,1381,1382. It is a highly adaptable test, not reliant on high technology, and is relevant for activities
of daily living.
The likely clinically significant improvement in ESWT is 85 seconds1383.
CONSTANT LOAD ENDURANCE ERGOMETRY
This test involves having the patient exercise on a treadmill or cycle ergometer at a fixed work rate1384. The
work rate is generally set at 75% to 85% of the individual’s Wmax established in a previous maximal
incremental exercise test, or it can be self-paced. The duration of the test is the primary outcome measure,
but Borg ratings of dyspnoea and effort or fatigue, and oxygen saturation can usefully be added.
Endurance walk tests performed on a treadmill compare closely with those performed in a corridor walking
test, but measurements are easier to make in a treadmill test1385, and it is not subject to vagaries of traffic
flow and ambient conditions that potentially can affect corridor walk tests. On the other hand, treadmills
are expensive, space-consuming, and often daunting to patients with severe disease or advanced years.
Attempts to compare the two have produced inconsistent results in terms of equivalence of energy
expenditure and endurance performance1386,1387.
1376
Pinto-Plata, Cote C, Cabral H, et al. The 6-min walk distance: change over time and value as a predictor of
survival in severe COPD. Eur Respir J 2004; 23:28-33
1377
Celli BR, Cote CG, Mariv JM, Casanova C, et al. The BMI, airflow obstruction, dyspnea and exercise capacity
index in COPD. New Engl J Med 2004; 350:1005-1012
1378
Revill SM, Morgan MDL, Singh SJ, Williams J, Hardman AE. The endurance shuttle walk: a new field test for
the assessment of endurance capacity in chronic obstructive pulmonary disease. Thorax 1999; 54:213-222
1379
Eaton T, Young P, Nicol K, Kolbe J. The endurance shuttle walking test: a responsive measure in pulmonary
rehabilitation for COPD patients. Chron Respir Dis 2006; 3:3-9
1380
Pepin V, Brodeur J, Lacasse Y, et al. Six-minute walking versus shuttle walking : responsiveness to
bronchodilation in chronic obstructive pulmonary disease. Thorax 2007; 63:291-298
1381
Pepin V, Saey D, Whittom F, LeBalnc P, Maltais F. Walking versus cycling: sensitivity to bronchodilation in
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2005; 172:1517-1522
1382
Brouillard C, Pepin V, Milot J, Lacasse Y, Maltais F. Endurance shuttel walking test : responsiveness to
salmeterol in COPD. Eur Respir J 2008; 31:579-584
1383
Brouillard C, Pepin V, Singh S, Revill SM, Lacasse Y, Maltais F. Interpreting changes in endurance shuttle
walking performance. Am J Respir Crit Care Med 2007; 175:A367
1384
Beaumont A, Cockcroft A, Guz A. A self paced treadmill walking test for breathless patients. Thorax 1985;
40:459-464
1385
Swerts PMJ, Mostert R, Wouters EFM. Comparison of corridor and treadmill walking in patients with severe
chronic obstructive pulmonary disease. Phys Ther 1990; 70:439-442
1386
Pearce ME, Cunningham DA, Donner AP, et al. Energy cost of treadmill and floor walking at self-selected paces.
Eur J Appl Physiol Occup Physiol 1983; 52:115-119
1387
Stevens D, Elpern E, Sharma K, Szidon P, et al. Comparison of hallway and treadmill six-minute walk tests. Am J
Respir Crit Care Med 1999; 160:1540-1543
167
Nutritional Impairments
Patients with severe COPD often lose weight1388. In a large (n=1612) uncontrolled cohort study, loss of
over 1 unit of body mass index (BMI) was as frequent as 35.3% in females and 27.4% in males in the
presence of severe COPD1389. A smaller cohort study found the prevalence of under-nutrition was
24.4%1390.
Weight under 90% of ideal or weight loss of 5% to 10% of initial body weight are considered indices of
malnutrition, and these features have been described in 24% to 35% of patients with moderate and severe
COPD1391. Low body weight is associated with more severe breathlessness for the same severity of lung
function impairment1392. Such a relative catabolic state has been shown in a number of uncontrolled cohort
1393,1394,1395,1396
or retrospective studies to be an independent risk factor for worse prognosis
. Low body
1397
mass index (BMI ) is an independent predictor of survival , and affects mortality due to both COPD and
all-causes1398,1399. BMI <20 also relates to lung function – FEV1 and gas transfer – and maximum
inspiratory pressure as an indicator of diaphragmatic strength, as well as level of dyspnoea1400. An
uncontrolled cohort study found that BMI, fat free mass and muscle mass were lowest in COPD patients
with chronic hypoxaemia, or in those with severe impairment of FEV1 (independent of their oxygenation
status)1401.
Correlates of nutrition (e.g. thigh muscle wasting and hand-grip strength) are also powerful independent
prognostic indicators1402, but are further strengthened by inclusion of FEV1 as percent predicted1403. Fatfree body mass has been more closely correlated with respiratory muscle strength and functional walking
tests than percent ideal body weight1404. While peak exercise performance was compromised in
1388
Hunter AMB, Carey MA, Larsh HW. The nutritional status of patients with chronic obstructive pulmonary
disease. Am Rev Respir Dis 1981; 124:375-381
1389
Prescott E, Almdal T, Mikkelsen KL, Tofteng CL, et al. Prognostic value of weight change in chronic obstructive
pulmonary disease: results from the Copenhagen City Heart Study. Eur Respir J 2002; 20:539-544
1390
Gray-Donald K, Gibbons L, Shapiro SH, Martin JG. Effect of nutritional status on exercise performance in
patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1989; 140:1544-1548
1391
Congleton J. The pulmonary cachexia syndrome. Proc Nutr Soc 1999; 58:321-328
1392
Sahebjami H, Sathianpitayakul E. Influence of body weight on the severity of dyspnea in chronic obstructive
pulmonary disease. Am J Respir Crit Care Med 2000; 161:886-890
1393
Traver GA, Cline MG, Burrows B. Predictors of mortality in chronic obstructive pulmonary disease. Am Rev
Respir Med 1979; 119:895-902
1394
Wilson DO, Rogers MR, Wright EC, et al. Body weight in chronic obstructive pulmonary disease. Am Rev Respir
Dis 1989; 139:1435-1414
1395
Chailleux E, Fauroux B, Binet F, et al. Predictors of survival in patients receiving domiciliary oxygen therapy or
mechanical ventilation: a 10-year analysis of ANTADIR Observatory. Chest 1996; 109:741-749
1396
Landbo C, Prescott E, Lange P, et al. Prognostic value of nutritional status in chronic obstructive pulmonary
disease. Am J Respir Crit Care Med 1999; 160:1856-1861
1397
Landbo C, Prescott E, Lange P, et al. Prognostic value of nutritional status in chronic obstructive pulmonary
disease. Am J Respir Crit Care Med 1999; 160:1856-1861
1398
Landbo C, Prescott E, Lange P, et al. Prognostic value of nutritional status in chronic obstructive pulmonary
disease. Am J Respir Crit Care Med 1999; 160:1856-1861
1399
Prescott E, Almdal T, Mikkelsen KL, Tofteng CL, et al. Prognostic value of weight change in chronic obstructive
pulmonary disease: results from the Copenhagen City Heart Study. Eur Respir J 2002; 20:539-544
1400
Sahebjami H, Doers JT, Render ML, Bond TL. Anthropometric and pulmonary function test profiles of
outpatients with stable chronic obstructive pulmonary disease. Am J Med 1993; 94:469-474
1401
Schols AMWJ, Soeters PB, Dingemans AMC, Mostert R, et al. Prevalence and characteristics of nutritional
depletion in patients with stable COPD eligible for pulmonary rehabilitation. Am Rev Respir Dis 1993; 147:11511156
1402
Engelen MP, Schols AM, Baken WG, et al. Nutritional depletion in relation to respiratory and peripheral skeletal
muscle function in out-patients with COPD. Eur Respir J 1994; 7:1793-1797
1403
Marquis K, Debigare R, Lacasse Y, LeBlanc P, et al. Midthigh muscle cross-sectional area is a better predictor of
mortality than body mass index in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med
2002; 166:809-813
1404
Schols AMWJ, Soeters PB, Dingemans AMC, Mostert R, et al. Prevalence and characteristics of nutritional
depletion in patients with stable COPD eligible for pulmonary rehabilitation. Am Rev Respir Dis 1993; 147:11511156
168
underweight people with COPD, neither submaximal exercise performance nor health status were1405. Peak
VO2 has been correlated with fat free mass, BMI and intracellular water1406.
As well as cross-sectional indices of body mass weight loss also has prognostic significance1407. Weight
loss is common in COPD patients – up to 32% of underweight patients had lost >5% of body weight in the
year before study1408. In a prospective study examined post hoc, history of weight loss correlated with
decreased survival, and weight gain in both under-nourished and those with normal weight was associated
with decreased risk of mortality1409. This latter finding has been replicated1410.
To summarise these observations, weight loss may occur in a third of people with severe COPD, and both
absolute weight and weight loss (and their more accurate correlates of nutritional status, BMI, fat free mass
and skeletal muscle strength) are strong indicators of mortality. If nutritional status can be improved,
survival may improve (along with exercise performance). It is therefore important to assess nutritional
status, muscle strength and recent weight loss before PR.
It might appear useful to embark on weight-maintenance early in the course of the disease, since nutritional
support later in disease has shown no significant gain in health status or exercise capacity in a metaanalysis that included 277 patients with stable severe COPD1411. Improvements in weight can be achieved
with supplementation, as documented in a small randomised controlled trial, though there were no
improvements in health status1412. In another intervention study that included repletion and anabolic
steroids, body weight increased along with fat free mass, inspiratory muscle strength and decreased risk of
early death, without adverse effects1413.
Nutritional Status
Body Mass Index
Body mass index (BMI) is a function simply of height and weight (weight in Kg / [height in metres]2), and
includes fat and fat-free mass. Significant muscle wasting can occur in people with normal or even high
BMI. BMI is a strong independent predictor of survival in COPD1414,1415, and gaining weight is associated
1405
Gray-Donald K, Gibbons L, Shapiro SH, Martin JG. Effect of nutritional status on exercise performance in
patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1989; 140:1544-1548
1406
Baarends EM, Schols AM, Mostert R, Wouters EF. Peak exercise response in relation to tissue depletion in
patients with chronic obstructive pulmonary disease. Eur Respir J 1997; 10:2807-2813
1407
Prescott E, Almdal T, Mikkelsen KL, Tofteng CL, et al. Prognostic value of weight change in chronic obstructive
pulmonary disease: results from the Copenhagen City Heart Study. Eur Respir J 2002; 20:539-544
1408
Gray-Donald K, Gibbons L, Shapiro SH, Martin JG. Effect of nutritional status on exercise performance in
patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1989; 140:1544-1548
1409
Schols AMWJ, Slangen J, Volovics L, Wouters EFM. Weight loss is a reversible factor in the prognosis of
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157:1791-1797
1410
Prescott E, Almdal T, Mikkelsen KL, Tofteng CL, et al. Prognostic value of weight change in chronic obstructive
pulmonary disease: results from the Copenhagen City Heart Study. Eur Respir J 2002; 20:539-544
1411
Ferreira IM, Brooks D, Lacasse Y, et al. Nutritional supplementation for stable chronic obstructive pulmonary
disease. (Cochrane Review). The Cochrane Library: Update Software 2003; Issue 3
1412
Otte KE, Ahlburg P, D’Amore F, Stellfield M. Nutritional repletion in malnourished patients with emphysema. J
Parenteral Enteral Nutr 1989; 13:152-156
1413
Schols AMWJ, Slangen J, Volovics L, Wouters EFM. Weight loss is a reversible factor in the prognosis of
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157:1791-1797
1414
Gray-Donald K, Gibbons L, Shapiro SH, et al. Nutritional status and mortality in chronic obstructive pulmonary
disease. Am J Respir Crit Care Med 1996; 153:961-966
1415
Landbo C, Prescott E, Lange P, et al. Prognostic value of nutritional status in chronic obstructive pulmonary
disease. Am J Respir Crit Care Med 1999; 160:1856-1861
169
with lower mortality1416,1417. As BMI is such a simple measure with such good independent risk prediction
properties it has been included in the BODE index, along with other major risk factors for survival1418.
Fat Free Mass
Indicators that reflect muscle mass depletion have appeal over BMI, and FFM more closely reflects
metabolically active “body cell mass”. FFM appears to be the main component of body mass contributing
to the associations with exercise limitation, quality of life and mortality. Patients with COPD whose lean
body mass (FFM) is depleted have the greatest impairment of HRQoL1419. Even in COPD patients with
normal BMI followed for 7 years in the Copenhagen City Heart Study, FFM was an independent predictor
of mortality1420.Some measures are indirect albeit reliable screening tools, while others are more accurate
and reliable although requiring significant technological investment.
MID-ARM MUSCLE AREA
MAMA is appealing as it is easily measured, and in a Spanish prospective cohort of 96 male COPD
patients, it provided better prognostic information than BMI1421.
SKINFOLD THICKNESS
ST measured at four sites (triceps, biceps, subscapular and supra-iliac) is a time-honoured tool, in which
fat-mass is obtained from equations or tables. FFM is body weight minus fat-mass1422.
NON-FAT NON-BONE MASS
Dual-energy X-ray absorptiometry (DEXA)1423 DEXA measures non-fat, non-bone mass. The equipment
is the same as that used for Bone Mineral Density measurements, though the computations are different for
FFM.
BIOELECTRICAL IMPEDANCE
Bioimpedance analysis1424. measures fat free mass, and new technological tools are becoming less
expensive and more widely available, meaning more routine use in respiratory patients is becoming a more
realistic possibility.
Nutritional Screening Measures
Patient-Generated Subjective Global Assessment (PG-SGA) Tool
This tool has been validated in cancer patients1425,1426, and has been used in pulmonary rehabilitation
participants. The global rating provides categories of �well nourished’, �moderate or suspected
1416
Schols AM, Slangen J, Volovics L, Wouters EF. Weight loss is a reversible factor in the prognosis of chronic
obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 157:1791-1797
1417
Prescott E, Almdal T, Mikkelsen KL, Tofteng CL, et al. Prognostic value of weight change in chronic obstructive
pulmonary disease: results from the Copenhagen City Heart Study. Eur Respir J 2002; 20:539-544
1418
Celli BR, Cote CG, Marin JM, Casanova C, et al. The body-mass index, airflow obstruction, dyspnea, and
exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med 2004; 350:1005-1012
1419
Mostert R, Goris A, Weling-Scheepers C, et al. Tissue depletion and health related quality of life in patients with
chronic obstructive pulmonary disease. Respir Med 2000; 94:859-867
1420
Vestbo J, Prescott E, Almdal T, Dahl M, et al. Body mass, fat-free mass, and prognosis in patients with chronic
obstructive pulmonary disease from a random population sample. Findings from the Copenhagen City Heart Study.
Am J Respir Crit Care Med 2006; 173:79-83
1421
Soler-Cataluna JJ, Sanchez-Sanchez L, Martinez-Garcia MA, et al. Mid-arm muscle area is a better predictor of
mortality that body mass index in COPD. Chest 2005; 128:2108-2115
1422
Durnin JVGA, Womersley J. Body fat assessed from total body density and its estimation from skinfold
thickness: measurements on 481 men and women aged from 16 to 72 years. Br J Nutr 1974; 32:77-97
1423
Engelen MPKJ, Schols AMWJ, Heidendal GAK, Wouters EFM. Dual-energy X-ray absorptiometry in the clinical
evaluation of body composition and bone mineral density in patients with chronic obstructive pulmonary disease. Am
J Clin Nutr 1998; 68:1298-1303
1424
Lukaski HC, Johnson PE, Bolonchuk WW, Lykken GI. Assessment of fat-free mass using bioelectrical
impedance measurements of the human body. Am J Clin Nutr 1985; 41:810-817
170
malnutrition’ or �severely malnourished’, based on a patient-completed series of questions and an
observer-completed section.
Mini Nutritional Assessment (MNA)
This tool poses a series of questions relating to lifestyle, mobility and other global factors, dietary factors
such as protein intake, meal patterns etc, self-perceived nutritional and health status and anthropometric
measures, including self-reported weight loss. It has been validated in people aged over 65 years1427,1428.
Psychological Impairments
A wide range of questionnaires has been developed over the past 50 years to measure psychological
impairment. Their relative usefulness relates to their validity, reliability, responsiveness, generalisability,
and ease of use. Some are generic screening instruments (eg the General Health Questionnaire, Brief
Symptom Inventory and Symptom Checklist 90), while others address a range of transient mood states (eg
Profile of Mood States, and the Hospital Anxiety and Depression Scale). Yet others focus specifically on
personality (eg Minnesota Multiphasic Personality Inventory), tendency to depression (eg Beck Depression
Inventory, Centre for Epidemiological Studies Depression Mode Scale, and the Geriatric Depression
Scale), denial (Denial Rating Scale) or anxiety disorders (eg State Trait Anxiety Scale).
The impact of the psychological impairment on health status is considered elsewhere, but can be
determined from the generic Medical Outcomes Study Short Form surveys (eg SF36 and SF20), the
Nottingham Health Profile, or the Quality of Well-Being Scale questionnaires. The impact of
psychological status on breathing is addressed in most respiratory disease-specific health status
instruments, but other instruments that examine a person's control and coping systems can also be used.
These are detailed below (in alphabetical order). The impact of another somatic illness on psychological
status can be assessed from the Sickness Impact Profile or Psychosocial Adjustment to Illness Scale. Some
health status questionnaires also include psychological or mental health status, and some include
components that reflect degree of mastery or self-efficacy.
Beck Depression Inventory (BDI)1429 and BDI-Short Form1430
A 21-item self-administered questionnaire that takes 5 to 10 minutes to complete. It performs well as a
screen for clinically significant symptoms of depression, and has been used in many populations and a
variety of settings. When using this scale to assess people with chronic lung disease caution should be
exercised in the interpretation of results due to the emphasis on somatic symptoms.
Brief Symptom Inventory1431
The BSI is a shorter but psychometrically acceptable derivation from the SCL-90-R. Internal consistency
and test-retest reliability are good, and correlations with the symptoms dimension of the SCL-90-R are
quite high. There is also high convergence between BSI scales and similar dimensions of the MMPI.
1425
Isenring E, Bauer J, Capra S. The scored Patient-Generated Subjective Global Assessment (PGSGA) and its
association with quality of life in ambulatory patients receiving radiotherapy. Eur J Clin Nutr 2003; 57:305-309
1426
Bauer J, Capra S, Ferguson M. Use of the scored Patient-Generated Subjective Global Assessment (PG-SGA) as a
nutrition assessment tool in patients with cancer. Eur J Clin Nutr 2002; 56:779-785
1427
Guigoz Y, Vellas B, Garry PJ. Mini nutritional assessment: a practical assessment tool for grading the nutritional
state of elderly patients. S Gerontol 1994; Suppl 2: 15-60
1428
Bleda M, Bolibar I, Pares R, Salva A. Reliability of the mini nutritional assessment (MNA) in institutionalized
elderly people. J Nutr Health Aging 2002; 6:134-137
1429
Beck AT. Depression inventory. Philadelphia, PA: Center for Cognitive Therapy 1978
1430
Reynolds WM, Gold JW. A psychometric investigation of the standard and short form Beck Depression
Inventory. J Consult Clin Psychol 1981; 49:306-307
1431
Derogatis LR, Spencer PM. Brief Symptom Inventory. Riderwood, MD: Clinical Psychometric Research 1982
171
Centre for Epidemiological Studies - Depression Mode Scale (CES-D)1432
This scale may be particularly suited to COPD as it places less emphasis on somatic symptoms of
depression, which may be confounded by respiratory impairments. It contains 20 items and takes around 5
to 10 minutes to self-administer. It has been tested in a broad range of populations and clinical settings. It
registers depressive symptoms, rather than providing a diagnostic formula for clinical depression. In a
large survey in Dutch general practices there was a 2.5-fold higher risk of these symptoms in severe COPD
than in age-matched demographically similar controls1433. In a large randomised trial, comprehensive PR
and education-only PR had similar benefits on depression scores using this scale1434. Thus, it has sensitivity
and responsiveness for depressive symptomatology in COPD.
COPD Self-Efficacy Scale (CSES)1435
Self-efficacy refers to the conviction people have as to whether they can carry out behaviours to achieve
certain outcomes. People suffering dyspnoea with activities learn to avoid those activities1436. A lack of
confidence in the ability to achieve outcomes from those activities is referred to as low self-efficacy. The
CSES is a 34-item questionnaire that takes 5 to 10 minutes of self-completion measures this self-efficacy,
specifically related to the limitations perceived as due to COPD. Five factors are identified - negative
affect, intense emotional arousal, physical exertion, weather/environmental and behavioural risk factors.
The questionnaire is validated in small groups, and its wider reliability and responsiveness to interventions
is uncertain.
General Health Questionnaire (GHQ 60, GHQ 30, GHQ 28)1437,1438,1439
The GHQ comes as 60-, 30- and 28-item self-administered questionnaires, which take patients 10, 5 and 5
minutes respectively to complete. It addresses the following domains - Somatic Symptoms, Anxiety and
Insomnia, Social Dysfunction, and Severe Depression. It was developed as a screening tool to detect
psychiatric disorders among general psychiatric outpatients and those in the community. It focuses on two
main areas: inability to carry out normal functions and appearance of new distressing phenomena.
Geriatric Depression Scale (GDS)1440
This 30-item self-administered scale takes 5 minutes to complete, and is well suited to elderly patients
(who make up most of the COPD population). A shorter version has also been developed1441. Record of its
use in respiratory disease has not been found.
1432
Radloff L. The CES-D: A self-report depression scale for research in the general population. Appl Psychol
Measur 1977; 1:385-401
1433
van Manen JG, Bindels PJE, Dekker FW, Ilzermans CJ, et al. Risk of depression in patients with chronic
obstructive pulmonary disease and its determinants. Thorax 2002; 57:412-416
1434
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995; 122:823-832
1435
Wigal JK, Creer TL, Kotses H. The COPD self-efficacy scale. Chest 1991; 99:1193-1196
1436
Bandura AB. Social learning theory. Englewood Cliffs, NJ; Prentice-Hall, Inc. 1977
1437
Goldberg DP, Blackwell B. Psychiatric illness in general practice. A detailed study using a new method of care
identification. Br Med J 1970; 11:439-443
1438
Goldberg P. The detection of psychiatric illness by questionnaire: a technique for the identification and
assessment of non-psychotic psychiatric illness. London: Oxford University Press 1972 (Maudsley Monographs No
21)
1439
Viewig BW, Hedlund JL. The general health questionnaire (GHQ): a comparative review. J Psychiatry 1983;
14:74-81
1440
Yesavage JA, Brink TL, Rose TL, Lum O, et al. Development and validation of a geriatric depression screening
scale: a preliminary report. J Psychiatric Res 1982; 17:37-49
1441
Brink TL, Yesavage JA, Lum O, Heersema PH, et al. Screening tests for geriatric depression. Clinical
Gerontologist 1982; 1:37-43
172
Hospital Anxiety and Depression Scale (HADS)1442,1443
This 14-item self-administered questionnaire takes around 5 to 10 minutes to complete, and is a useful
screen for clinically significant symptoms or anxiety and depression. It has been utilised in a variety of
populations and settings. It is capable of detecting either anxiety or depression in COPD populations and
appears responsive to interventions like PR1444.
Minnesota Multiphasic Personality Inventory (MMPI-2)1445
This is a rather daunting but highly validated, reliable and widely used self-administered questionnaire. It
has 567 questions that take 90 minutes or so to complete, and addresses a number of domains. There are 8
validity scales with 5 superlative self-presentation subscales, 10 clinical scales with 31 clinical subscales
(Harris-Lingoes and Social Introversion subscales), 15 Content scales, 27 Content Component scales, 25
supplementary scales and various special or setting-specific indices. It is used to measure psychopathology
across a broad range of client settings, and can help to diagnose personality syndromes as well as
psychopathology.
Multi-Dimensional Health Locus of Control (MHLC)1446
Form C of the MHLC is a condition-specific 18-item 5-minute self-administered questionnaire, which has
undergone extensive validation in a range of chronic diseases and cancers, showing high levels of
concurrent and construct validity as well as reliability and stability. The three scales are
internality/personal control, chance, and powerful others/professional control, and appear to be
independent1447. Sensitivity in respiratory diseases has not been reported.
Nottingham Health Profile1448,1449
This 38-item questionnaire can be self-administered or interviewer administered, and takes 5 to 10 minutes
to complete. The dimensions evaluated are Physical mobility, Pain, Social isolation, Emotional reactions,
Energy and Sleep, and there may be some confounding from somatic respiratory problems. It is widely
used, has been tested in a wide range of settings, and extensively validated. However, its responsiveness to
interventions for COPD is not clearly established.
Profile of Mood States (POMS)1450
This 65-item self-administered questionnaire takes around 5 minutes to complete (yes-no responses), and
assesses domains of Tension-anxiety, Depression-dejection, Anger-hostility, Vigour-activity, Fatigueinertia, Confusion-bewilderment. Surprisingly few studies have examined its responsiveness to
interventions in respiratory diseases.
1442
Zigmond AS, Snaith RP. The Hospital Anxiety and Depression Scale. Acta Psychiatr Scand 1983; 67:361-370
Bjelland I, Dahl AA, Haug TT, Neckelmann D. The validity of the Hospital Anxiety and Depression Scale. An
updated literature review. J Psychosom Res 2002; 52:69-77
1444
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at 1 year of outpatient multidisciplinary
pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
1445
MMPI-2 Manual for Administration, Scoring, and Interpretation Revised Edition
1446
Wallston KA. Stein MJ. Smith CA. Form C of the MHLC scales: a condition-specific measure of locus of control.
J Personality Assess 1994; 63:534-553
1447
Russell SF, Ludenia K. The psychometric properties of the Multidimensional Health Locus of Control Scales in
an alcoholic population. J Clin Psychol 1983; 39:453-459
1448
Hunt SM, McEwen J, McKenna SP. Measuring health status: a new tool for clinicians and epidemiologists. J Roy
Coll Gen Pract 1985; 35:185-188
1449
Prieto L, Alonso J, Ferrer M, Anoto JM. Are results of the SF-36 health survey and the Nottingham Health Profile
similar? A comparison in COPD patients. Quality of Life in COPD Study Groups. J Clin Epidemiol 1997; 50:463473
1450
McNair DM, Lorr M, Dropplemann LF. Profile of Mood States. San Diego, CA: Educational and Industrial
Testing Service 1971
1443
173
Psychosocial Adjustment to Illness Scale (PAIS)1451
This questionnaire is answered in a semi-structured clinical interview, and requires a clinical psychologist
in attendance. It assesses the psychological and social adjustment of medical patients and/or members of
their immediate families to illness. Its reliability and validity have been well tested in a variety of
populations and clinical settings, including respiratory disease. Patients entering PR were assessed
clinically and with PAIS-Self Report to demonstrate validity, but also to show greater sensitivity for PAISSR in detecting the impact of COPD on patients1452.
Sickness Impact Profile (SIP)1453,1454,1455
This is a 136-item questionnaire that can be self-administered or interviewer administered. It takes 20 to 30
minutes to complete. The domains examined are Physical (ambulation, mobility, body care and
movement), and Psychosocial (social interaction, communication, alertness behaviour, emotional
behaviour, sleep and rest, eating, home management, recreation and pastimes, and enjoyment. It is
therefore one of the more comprehensive instruments to evaluate social as well as physical and
psychological issues, and has been used in a broad range of respiratory groupings, being suited to COPD,
asthma, cystic fibrosis, sarcoidosis and chronic respiratory failure patients. While it is described as
responsive, it is relatively insensitive to impacts of mild or moderate COPD.
State Trait Anxiety Scale1456
This self-administered questionnaire examines the dimensions of Anxiety proneness (trait) and Current
tension/apprehension (state). It has been tested widely and validated in many populations and settings. It
has 40 items and takes most people 10 minutes to complete. Its sensitivity to relaxation therapy reducing
anxiety and dyspnoea has been demonstrated1457, and in this study anxiety correlated with dyspnoea at all
time points. A randomised controlled study published as a PhD thesis has shown that while hope improved
with relaxation and coping training, no effect was seen in anxiety1458. No specific references to
responsiveness to PR were found.
Symptom Checklist 90 Revised (SCL-90-R)1459
This is a 90-item self-administered questionnaire with nine primary symptom dimensions and 3 global
indices. It is said to take around 15 minutes for the average patient to complete. Reliability and validity
have been tested in a wide range of populations and settings. It was designed (and performs well) to screen
for a broad range of psychological problems and symptoms of psychopathology. It has shown utility as a
primary indicator, an indicator of change over time, and as an outcomes measure following interventions.
1451
Derogatis LR. The psychosocial adjustment to illness scale (PAIS). J Psychosom Res 1986; 30:77-91
Stubbing DG, Haalboom P, Barr P. Comparison of the Psychosocial Adjustment to Illness Scale-Self Report and
clinical judgement in patients with chronic lung disease. J Cardiopulm Rehabil 1998; 18:32-36
1453
DeBruin A, DeWitte L, Stevens F, Diederiks J. Sickness impact profile: the state of the art of a functional status
measure. Soc Sci Med 1992; 35:1003-1014
1454
McSweeny AJ, Grant I, Heaton RK, et al. Life quality of patients with chronic obstructive lung disease. Arch
Intern Med 1982; 142:473-478
1455
White RJ, Rudkin ST, Ashley J, Stevens VAJ, et al. Outpatient pulmonary rehabilitation in severe chronic
obstructive pulmonary disease. J Roy Coll Phys London 1997; 31:41-55
1456
Speilberger CE, Gorusch RL, Luschene RE. Manual for the State-Trait Anxiety Inventory. Palo Alto, CA:
Consult Psychol Press 1970
1457
Renfroe KL. Effect of progressive relaxation on dyspnea and state anxiety in patients with chronic obstructive
pulmonary disease. Heart Lung 1988; 17:408-413
1458
Aubuchon BL. The effects of positive imagery on hope, coping, anxiety, dyspnoea and pulmonary function in
persons with chronic obstructive pulmonary disease: tests of a nursing intervention and a theoretical model. Uni
Texas Austin 1990 PhD thesis
1459
Derogatis LR. SCL-90-R: Administration, scoring, & procedures manual for the revised version. Baltimore:
Clinical Psychometric Research, 1983
1452
174
Ways of Coping Check List (WOCCL)1460
This is a 66-item self-administered questionnaire that takes around 10 minutes for most patients to
complete. It charts patients into a number of coping styles: confrontive, distancing, self-controlling,
seeking social support, accepting responsibility, escape-avoidance, active problem-solving and positive reappraisal. Its reliability and validity have been well tested in a variety of settings. It has been used in a
range of populations, and is useful for the assessment of behavioural and coping strategies used by people
in stressful situations.
5.3 Indicators of Functional Disability and
Handicap
Functional Exercise Endurance
Tests of respiratory function performed at rest help to provide insight into the degree of airway narrowing
or gas exchange impairment, but they give little understanding of the precise cause of a patient's inability
to perform activities. In particular, ventilatory requirements with these activities, limitations imposed by
cardiovascular impairments, and the role of pulmonary or peripheral vascular abnormalities in functional
capacity can only be determined by exercise testing (see above). Ergometry testing with ventilation and gas
exchange measurements can provide diagnostic information about exercise impairment1461.
While this information about impairments is valuable, the term impairment refers more to an injury or
abnormality occurring at the individual or organ system level representing “any loss or abnormality of
psychological, physiological, or anatomic structure or function”1462. Disability, on the other hand, refers
more to the effects of the impairments and their interplay and consequences on the individual's functional
capacity. Disability is defined as “any restriction or lack (resulting from an impairment of ability to
perform an activity in the manner or within the range considered normal for a human being”. The WHO
definitions also include handicap, which is the “disadvantage for a given individual that limits or prevents
the fulfilment of a role that is normal (depending upon age, sex, social and cultural factors) for that
individual”, though recent revisions now talk about "functional disability" which tends to combine
disability and handicap. There is therefore a variety of measurements that can reflect disability and
handicap as aspects of functional status, which has been defined as a person’s ability to perform ADLs
(comprising psychological, physical and social functioning)1463.
Observations of perceived exertion and dyspnoea1464, pulse and respiratory rate responses and oxygen
saturation during an exercise task provide useful insight into functional capacity. The exercise task may be
a standardised test (such as a timed walking test, ergometry-based endurance test, or supported and
unsupported arm exercise tests), which are standardised and validated, attractive properties for outcome
testing. Alternatively, they may grade performance tasks that cover a range of energy expenditures (eg
washing hands and face, changing bed linen, and heavier housework or gardening)1465. Breathing patterns
and task performance can also be assessed1466 during these task-related tests.
1460
Folkman S, Lazarus RS. J Personality Soc Psychol 1985; 48:150-170
Wasserman K. Exercise tolerance in the pulmonary patients. In: Principles and Practice of Pulmonary
Rehabilitation. Eds Casaburi R, Petty TL. Philadelphia: WB Saunders Company 1993, pp 115-123
1462
World Health Oganization. WHO international classification of impairments, disabilities and handicaps: a manual
of classification relating to the consequences of diseases. Geneva: World Health Organization 1980
1463
Lareau SC, Breslin EH, Meek PM, et al. Functional status instruments: Outcome measure in the evaluation of
patients with chronic obstructive pulmonary disease. Heart Lung 1996; 25:212-224
1464
Borg G. Psychophysical bases of perceived exertion. Med Sci Sports Exer 1982; 14:377-381
1465
Blair SN, et al. Guidelines for Graded Exercise Testing and Prescription. 3rd ed. Philadelphia: Lea & Febiger
1986
1466
Trombly C, Scott AD. Evaluation and assessment. In: Occupational Therapy for Physical Dysfunction. Baltimore:
Williams & Wilkins 1977
1461
175
Functional walk tests have been qualitatively reviewed recently1467. Fifty-two studies of measurement
properties were found in the review, most (twenty-nine) relating to the six-minute walk test, with fewer
studies of the 2-minute walk test (five), 12-minute walk test thirteen), shuttle walk test - both incremental
and endurance (four), and self-paced walk test (six). The six-minute walk test was favoured as the most
applicable to both clinical and research purposes due to its extensive validation and use in these settings.
The results are summarised, with the full references to be found in the qualitative review1468.
There are important influences in functional walking tests from encouragement, presence of a learning
effect, but not time of day of doing the test1469 (in either COPD or chronic heart failure). For each of the
timed walking tests patients should be given at least one trial to learn the test's requirements, with
sufficient recovery time between the trials; more than two tests do not appear to be necessary509,1470. The
tests appear valid measures of exercise capacity in various situations - COPD, cystic fibrosis, heart failure,
pacemakers, paediatrics, and surgical/pre-operative assessment. Strong to medium correlations have been
found in 28 studies between 6MWT and VO2max, maximum work capacity, and a variety of functional
and symptom measures1471. These included New York Heart Association functional classifications and
oxygen cost diagram. Results in heart failure also suggested some prognostic capacity for predicting
likelihood of death or hospitalisation for heart failure. Less clear correlations between 6MWT and healthrelated quality of life have been found in respiratory conditions. A recent study of 37 patients with severe
COPD and who completed a range of outcome measures before and 6 to 8 weeks after outpatient
comprehensive PR found a poor correlation between 6MWT and HRQoL results1472, even though each
measure showed clinically significant improvement. The 6MWT is responsive to interventions in a variety
of settings: correlation between 6MWT and diminished breathlessness after pacemaker insertion,
improvement in HRQoL in heart failure treatment, and HRQoL improvement after pulmonary
rehabilitation. The endurance shuttle walk test is more responsive to pulmonary rehabilitation than the
incremental shuttle walk test1473.
Functional Disability Questionnaires
(a)
Activities of Daily Living
The capacity of people to care for themselves and to actually perform ADL tasks are important aspects of
functional disability assessment. In Chronic Heart Failure (CHF), another common cause of chronically
disabling dyspnoea in older people, the New York Heart Association (NYHA) classes have wide
acceptance. The MRC Scales for Dyspnoea represent a good surrogate for functional disability, couched in
graded levels of activity that produce enough dyspnoea to limit the activity. Both basic and instrumental
ADL assessment (basic task capacity and performance ability respectively) have been combined in a
BADL-IADL, and validated in COPD as well as CHF.
Basic and Instrumental Activities of Daily Living Questionnaire (BADL-IADL)
In a multicentre Italian hospital study of 432 patients with CHF, 305 with COPD and 534 with diabetes
mellitus, validation was undertaken of a BADL-IADL assessment tool, and significant differences were
seen between the three conditions. In COPD a pattern of disablement with specific tasks (IADL) involving
1467
Solway S, Brooks D, Lacasse Y, Thomas S. A qualitative systematic overview of the measurement properties of
functional walk tests used in the cardiorespiratory domain. Chest 2001; 119:256-270
1468
Solway S, Brooks D, Lacasse Y, Thomas S. A qualitative systematic overview of the measurement properties of
functional walk tests used in the cardiorespiratory domain. Chest 2001; 119:256-270
1469
Guyatt GH, Pugsley SO, Sullivan MJ, Thompson PJ, et al. Effect of encouragement on walking test performance.
Thorax 1984; 39:818-822
1470
Guyatt GH, Sullivan MJ, Thompson PJ, Fallen EL, et al. The 6-min walk: a new measure of exercise capacity in
patients with chronic heart failure. Can Med Assoc J 1985; 132:919-923
1471
Solway S, Brooks D, Lacasse Y, Thomas S. A qualitative systematic overview of the measurement properties of
functional walk tests used in the cardiorespiratory domain. Chest 2001; 119:256-270
1472
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1473
Solway S, Brooks D, Lacasse Y, Thomas S. A qualitative systematic overview of the measurement properties of
functional walk tests used in the cardiorespiratory domain. Chest 2001; 119:256-270
176
mobility and outdoor activity, and practical involvement in household responsibility including money
management, with associated dependency was identified, rather than overall BADL1474. Responsiveness to
intervention has not yet been described, but this may a valuable disability indicator with potential for
outcome measurement.
Human Activity Profile (HAP)
This is a self-report questionnaire addressing 94 hierarchically-arranged VO2-demanding ADLs, designed
,
specifically for use in PR1475 1476, although little-used in this area1477. The HAP has good construct validity,
being closely associated with VO2max in patients attending PR (r=0.83)1478, and with directly-measured
activities from accelerometer over a week (r=0.78)1479. The sequential task-limitation arrangement allows
determination of a Maximal Activity Score (MAS), which is the greatest amount of work the patient is
currently able to perform (and actually performing at that time). The number of tasks then identified as
having been stopped because of dyspnoea is then subtracted from this MAS to provide an Adjusted
Activity Score (AAS). The AAS can be used to define low, fair, and average-and-above fitness levels, and
has been found to have good construct validity, repeatability and responsiveness to PR1480.
(b)
Health Status Measures
There has been considerable research and development activity in the area of health-related quality of life
(HRQoL) as a measure of disability and/or handicap in respiratory disease over the past 20 years. In the
Introduction section the differences between generic and disease-specific HRQoL were discussed. Briefly,
generic instruments classify a broad range of physical and psychological impairments and symptoms in
terms of their impact on health status, without reference to the disease causing the impairments or
symptoms. Use of such tools allows a comparison between different populations of health status - for
example comparing different chronic disease states (such as chronic heart failure, COPD and chronic renal
failure) or socio-demographic populations, and often they have been validated and normalised for different
age groups or ethno-cultural backgrounds. It has often been stated - and sometimes these statements have
been supported by objective research - that these instruments are not as sensitive to change (responsive) as
disease-specific measures.
Specific health status measures can be system-specific (eg respiratory disease as a whole) or diseasespecific (eg asthma, COPD, lung cancer, cystic fibrosis). It is more difficult to use these tools to compare
respiratory patients with cardiac or other patients. Using a system-specific tool it is feasible to compare
asthmatics with COPD patients, and so on, while using disease-specific tools reduces the capacity to
compare different diseases. On the other hand, it is usually stated that these tools are more responsive to
interventions.
(b.i) Generic Health Status Measures
1474
Incalzi RA, Corsonello A, Pedone F, Carbonin P, et al. Construct validity of activities of daily living scale. A clue
to distinguish the disabling effects of COPD and congestive heart failure. Chest 2005; 127:830-838
1475
Daughton DM, Fix AJ, Kass I, et al. Maximum oxygen consumption and the ADAPT quality of life scale. Arch
Phys Med Rehabil 1982; 63:620-622
1476
Fix AJ, Daughton DM. Human Activity Profile Professional Manual. Odessa FL: Psychological Assessment
Resources Inc; 1988
1477
Lareau SC, Breslin E, Meek P. Functional status instruments: outcome measure in the evaluation of patients with
chronic obstructive pulmonary disease. Heart Lung 1996; 25:212-224
1478
Daughton DM, Fix AJ, Kass I, et al. Maximum oxygen consumption and the ADAPT quality of life scale. Arch
Phys Med Rehabil 1982; 63:620-622
1479
Johansen KL, Painter P, Kent-Braun JA, et al. Validation of questionnaires to estimate physical activity and
functioning in end-stage renal disease. Kidney Internet 2001; 59:1121-1127
1480
Nield M, Hoo GS, Roper J, et al. Usefulness of the Human Activity Profile, a functional performance measure, in
people with chronic obstructive pulmonary disease. J Cardiopulm Rehabil 2005; 25:115-121
177
Medical Outcomes Survey (MOS) Questionnaire1481
This tool is in very wide use in Australia and many other countries. It can be self-administered or
interviewer administered (including by telephone1482), and there are computer versions available. It has
been validated in many populations at a range of ages, and there are extensive normal values for
Australia1483. It has been used in many chronic disease populations1484, including a variety of chronic
respiratory conditions1485.
MOS-Short Form 36, 20 and 9 Questionnaires (SF-36, SF-20, and SF-9)1486
These surveys take between 5 and 10 minutes to complete. The SF-20 has been examined alongside BDI
and lung function as a cross-sectional indicator of general health status1487. The BDI dyspnoea ratings
predicted general health status (SF-20). In another large Japanese cross-sectional study of 194 male
patients with stable COPD, there were significant gradations for most SF-36 dimensions across disease
severity groupings by ATS (FEV1) criteria, though there were substantial overlaps1488.
Because these instruments were designed to evaluate cross-sectional health status across populations, and
patients with COPD have low scores for a range of the dimensions, responsiveness to change is difficult to
identify ("floor effect"). In an uncontrolled observational study of patients undergoing comprehensive
outpatient PR, significant changes were seen in exercise performance, dyspnoea and mastery, as well as
overall HRQoL from the disease-specific CRDQ, but non-significant changes were found in SGRQ and
SF-36 (total and all nine health concepts)1489. Other studies have shown no or small improvements in SF36 or one or more of its components or summary scores1490,1491,1492,1493, though comparison of efficacy of
treatments for COPD with interventions in other conditions can be usefully made1494.
Quality of Well-Being Scale (QWB)1495
This is a comprehensive measure of health status, well validated1496 in a variety of clinical areas including
COPD. The original form is interviewer-administered (as a structured interview with 16 items), and takes
1481
Ware JF, Sherbourne CD. The MOS 36-Item Short Form Health Survey (SF-36). Conceptual framework and item
selection. Med Care 1992; 30:473-483
1482
Watson EK, Firman DW, Baade PD, Ring I. Telephone administration of the SF-36 health survey: validation
studies and population norms for adults in Queensland. Aust NZ J Publ Health 1996; 20:359-363
1483
McCallum J. The SF-36 in an Australian sample. Aust J Public Health 1995; 19:160-166
1484
Stewart AL, Greenfield S, Hays RD, Wells K, et al. Functional status and well-being of patients with chronic
conditions. J Am Med Assoc 1989; 262:907-913
1485
Mahler DA, Mackowiak JI. Evaluation of the short-form 36-item questionnaire to measure health-related quality
of life in patients with COPD. Chest 1995; 107:1585-1589
1486
Stewart AL, Hays RD, Ware JE. The MOS short-form general health survey: reliability and validity in a patient
population. Med Care 1988; 26:724-735
1487
Mahler DA, Faryniarz K, Tomlinson D, Colice GL, et al. Impact of dyspnoea and physiologic function on general
health status in patients with chronic obstructive pulmonary disease. Chest 1992; 102:395-401
1488
Hajiro T, Nishimura K, Tsukino M, Ikeda A, et al. A comparison of the level of dyspnea vs disease severity in
indicating the health-related quality of life of patients with COPD. Chest 1999; 116:1632-1637
1489
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1490
Benzo R, Flume PA, Turner D, Tempest M. Effect of pulmonary rehabilitation on quality of life in patients with
COPD: the use of SF-36 summary scores as outcome measures. J Cardiopulm Rehabil 2000; 20:231-234
1491
Boueri FM, Bucher-Bartelson BL, Glenn KA, Make BJ. Quality of life measured with a generic instrument (Short
Form-36) improves following pulmonary rehabilitation in patients with COPD. Chest 2001; 119:77-84
1492
Harper R, Brazier J, Waterhouse J, Walters S, et al. Comparison of outcome measures for patients with chronic
obstructive pulmonary disease (COPD) in an outpatient setting. Thorax 1997; 52:879-887
1493
Berry MJ, Rejeski WJ, Adair NE, Zaccaro D. Exercise rehabilitation and chronic obstructive pulmonary disease
stage. Am J Respir Crit Care Med 1999; 160:1248-1253
1494
Boueri FM, Bucher-Bartelson BL, Glenn KA, Make BJ. Quality of life measured with a generic instrument (Short
Form-36) improves following pulmonary rehabilitation in patients with COPD. Chest 2001; 119:77-84
1495
Kaplan RM, Atkins CJ, Timms R. Validity of a quality of well-being scale as an outcome measure in chronic
obstructive pulmonary disease. J Chronic Dis 1984; 37:85-95
1496
Anderson JP, Kaplan RM, Berry CC, et al. Interday reliability of function assessment for a health status measure.
The quality of well-being scale. Med Care 1989; 27:1076-1083
178
around 15 to 20 minutes to complete, but more recent development has led to a self-administered version
(QWB-SA). Scores cover symptoms, mobility, physical activity and social activity, and they can also be
used to develop utility (as QALYs) for health economic analysis. Responsiveness to intervention has been
described for cystic fibrosis and interstitial lung disease populations1497, though there are conflicting
reports of its use as an outcome measure in COPD1498,1499. In the latter study, a large randomised trial
comparing comprehensive PR with education-only with observation over six years, QWB scores at
baseline were a strong independent predictor of survival. In the National Emphysema Treatment Trial the
SF-36, QWB-SA, SGRQ and SOBQ were evaluated for responsiveness to PR. Both generic and both
disease-specific instruments were responsive, and they were interrelated1500.
(b.ii) Respiratory System Specific Health Status Measures
Air Index1501
This self-administered 63-item questionnaire usually takes 15 to 20 minutes to complete. It has four
dimensions - psychological, physical activity, physical symptoms, and social. It has been validated, but its
sensitivity and responsiveness to interventions have not been published.
Airways Questionnaire 20-item (AQ20)1502,1503
This brief questionnaire takes only 2 to 3 minutes to answer, having a yes/no answer format and only 20
questions, and is just as easy to score. It was developed at St George's Hospital London along similar
development lines as the SGRQ. It can be used for both asthma and COPD, and its brevity suggests it
could be used more routinely as a clinical tool, as well as being validated for research work. Its
responsiveness to intervention has not been published.
Asthma Quality of Life Questionnaire (AQLQ)
The AQLQ was derived along the same lines as the CRDQ for use in patients with asthma. Like the CRDQ
it was originally developed for interviewer administration1504, then as a self-administered questionnaire.
There are 32 items, which take around 10 to 15 minutes to complete, and covers symptoms, emotions,
exposures to environmental triggers, and activity limitation. It is available in a variety of languages. It has
been extensively validated, and is responsive to intervention1505,1506.
1497
Chang JA, Curtis JR, Patrick DL, Raghu G. Assessment of health-related quality of life in patients with interstitial
lung disease. Chest 1999; 116:1175-1182
1498
Guyatt GH, King DR, Feeny DH, et al. Generic and specific measurements of health-related quality of life in a
clinical trial of respiratory rehabilitation. J Clin Epidemiol 1999; 52:187-192
1499
Ries AL, Kaplan RM, Limberg TM, Prewitt LM. Effects of pulmonary rehabilitation on physiologic and
psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 1995; 122:823-832
1500
Kaplan RM, Ries AL, Reilly J, Mohsenifar Z, for the NETT Research Group. Measurement of health-related
quality of life in the National Emphysema Treatment Trial. Chest 2004; 126:781-789
1501
Letrait M, Lurie A, Bean K, Mesbah M, Venot A, Strauch G, et al. The Asthma Impact Record (AIR) Index: a
rating scale to evaluate the quality of life of asthmatic patients in asthma. Eur Respir J 1996; 9:1167–73
1502
Barley EA, Quirk FH, Jones PW. Asthma health status in clinical practice: validity of a new short and simple
instrument. Respir Med 1998; 92:1207-1214
1503
Hajiro T, Nishimura K, Jones PW, Tsukino M, Ikeda A, Koyama H, Izumi T. A novel, short and simple
questionnaire to measure health-related quality of life in patients with chronic obstructive pulmonary disease. Am J
Respir Crit Care Med 1999; 159:1874-1878
1504
Juniper EF, Guyatt GH, Epstein RS, Ferrie PJ, et al. Evaluation of impairment of health-related quality of life in
asthma: development of a questionnaire for use in clinical trials. Thorax 1992;47:76-83
1505
Toneguzzi RC, Population Medicine Group 91C. Self-management, autonomy, and quality of life in asthma.
Chest 1995;107:1003-1008
1506
Boulet L, Boutin H, Cote J, et al. Evaluation of an asthma self-management education program. J Asthma
1995;32:199-206
179
Asthma Quality of Life Questionnaire (Marks)1507
This simple questionnaire, developed in Australia and extensively validated, takes around 5 minutes for
patients to complete the 20 questions. It covers breathlessness and physical restrictions, mood disturbance,
social disruption, and personal concerns for health. It appears responsive to changes in asthma status1508.
Breathing Problems Questionnaire (BPQ)1509,1510
This self-administered 33-item or 10-item (Short-version) questionnaire is available in a variety of
languages and takes around 3 to 10 minutes to complete. It has 13 domains, scored in two constructs health knowledge and health appraisal. It appears responsive to change after PR1511.
Chronic Respiratory Disease Questionnaire (CRDQ)
The CRDQ was developed to determine effects of respiratory disease on health status, and its change
following interventions1512. It was originally designed for interviewer administration, and is therefore
rather resource intensive, though recent adaptations have been made that allow self-administration. It is
available in several languages, and has been validated in them all. It is really a system-specific instrument
rather than disease-specific, and has been used in COPD, asthma, and cystic fibrosis.
There are 123 questions that relate to health status over the past two weeks, measured on a 7-point Likert
scale, which contribute to four component scores: Dyspnoea, Emotional Function, Fatigue and Mastery,
but the four components can be summed to provide a total score of 20 to 140. In answering the Dyspnoea
component the patient is asked to identify the five tasks or activities important to their everyday life that
make them feel breathless, then indicate how severely breathless they are with each activity. When
answering a follow-up questionnaire, the patient is reminded of their first score for each question, so they
can more clearly indicate a direction of change. Because each patient chooses his/her own dyspnoeacausing activities, he/she cannot be compared to other patients.
This instrument has been used to define a population's health status related to respiratory disease, in which
circumstance it performs in a similar way to other health status measurements. For example, when
compared with SGRQ and several dyspnoea measures in 160 male Japanese patients with mild to severe
COPD, the Dyspnoea component grouped with the specific dyspnoea measures and SGRQ Activities
dimension in factor analysis. On the other hand, the CRDQ Emotional function component did not group
with HADS but with "other HRQoL" (together with CRDQ Fatigue and Mastery, and SGRQ Symptoms
dimension)1513. In another study of 100 UK patients with COPD, the Dyspnoea component score showed
poor correlation with MRC Dyspnoea Grade, while the other components related closely with SGRQ, and
there were significant differences between MRC Dyspnoea Grades1514 for Fatigue and Mastery
components. A comprehensive controlled study in elderly men with COPD (n=96) compared to 55 older
men with normal lung function1515. Both the BPQ and the CRDQ were repeatable, but BPQ was more
1507
Marks GB, Dunn SM, Woolcock AJ. A scale for the measurement of quality of life in adults with asthma. J Clin Epidemiol
1992;45:461-472
1508
Marks GB, Dunn SM, Woolcock AJ. An evaluation of an asthma quality of life questionnaire as a measure of change in adults
with asthma. J Clin Epidemiol 1993; 46:1103-1111
1509
Hyland ME, Bot J, Singh S, Kenyon CAP. Domains, constructs and the development of the Breathing Problems
Questionnaire. Qual Life Res 1994; 3:245-256
1510
Hyland ME, Singh SJ, Sodergren SC, Morgan MP. Development of a shortened version of the Breathing
Problems Questionnaire suitable for use in a pulmonary rehabilitation clinic: a purpose-specific, disease-specific
questionnaire. Qual Life Res 1998; 7:227-233
1511
Singh SJ, Smith DL, Hyland ME, Morgan MD. A short outpatient pulmonary rehabilitation programme:
immediate and longer-term effects on exercise performance and quality of life. Respir Med 1998;92:1146-1154
1512
Guyatt GH, Berman LB, Townsend M, et al. A measure of quality of life for clinical trials in chronic lung disease.
Thorax 1987; 42:773-778
1513
Hajiro T, Nishimura K, Tsukino M, Ikeda A, et al. Analysis of clinical methods used to evaluate dyspnea in
patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998; 158:1185-1189
1514
Bestall JC, Paul EA, Garrod R, Garnham R, et al. Usefulness of the Medical Research Council (MRC) dyspnoea
scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 1999; 54:581-586
1515
Yohannes AM, Roomi J, Waters K, Connolly MJ. Quality of life in elderly patients with COPD: measurement
and predictive factors. Respir Med 1998; 92:1231-1236
180
sensitive than CRDQ in these older British men. The most important determinants of CRDQ were
activities of daily living (NEADL) and emotional status in this study. Depression scores, exercise
limitation and dyspnoea-related limitation were the main factors accounting for level of HRQoL in
CRDQ1516.
The CRDQ was designed to be responsive to intervention, and it has performed well in demonstrating
changes following PR, as a total HRQoL score and as individual component scores1517,1518,1519,1520. Indeed,
in a small prospective study of PR, CRDQ was one of three most responsive objective outcome measures
(with BDI/TDI and 6MWD)1521. Given these discriminant properties, the CRDQ should be highly
recommended for use as an outcome measure for both research and routine clinical purposes. The
drawback of requiring a trained interviewer for each patient appears to have been surmounted with a selfcompletion form, which has been found to be as sensitive to change with PR as the interview-based
form1522.
Living With Asthma Questionnaire (LWAQ)1523
Hyland described this 68-item questionnaire in 1991. Its length may be a deterrent to more widespread use
- it takes around 20 minutes to complete, either self-administered or conducted by a trained interviewer. Its
validity, reliability and responsiveness have been demonstrated. There are many dimensions addressed,
including sport, social/leisure, holidays, sleep, mobility, work/other activities, colds, effects on others, sex,
medication usage, and dysphoric states and attitudes.
Maugeri Foundation Respiratory Failure Questionnaire (MRF28)1524
This 28-item questionnaire was designed for use in chronic respiratory failure in people with COPD or
kyphoscoliosis. It is available in several languages, takes about 10 minutes to complete (self-administered),
and evaluates daily activities, cognitive and emotional status, invalidity, perceptions of health, and
respiratory health. It discriminates well between different stages of severity of disease, and is the only
validated instrument for evaluating these issues in people with chronic respiratory failure.
Pulmonary Function Status and Dyspnoea Questionnaire (PFSDQ)
This measure has been validated to measure breathlessness with activities and changes in functional
ability1525. It has 164 items, presenting 79 activities of daily living that the patient nominates intensity of
dyspnoea associated with them as well as any alteration in their functional ability to perform them as a
result of their COPD. It does rely on patient memory, as it seeks their experiences over the past 30 days.
Activities are relevant for adults of either gender, reflecting a range of energy requirements, grouped into
scales of self-care, mobility, eating, home management, social and recreational. Validation shows good
1516
Engstrom CP, Persson LO, Larsson S, Sullivan M. Health-related quality of life in COPD: why both diseasespecific and generic measures should be used. Eur Respir J 2001; 18:69-76
1517
Wijkstra PJ, Tenvergert EM, VanAltena R, Otten V, et al. Reliability and validity of the Chronic Respiratory
Questionnaire (CRQ). Thorax 1994; 49:465-467
1518
Goldstein RS, Gort EH, Stubbing D, et al. Randomized controlled trial of respiratory rehabilitation. Lancet 1994;
344:1394-1397
1519
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at 1 year of outpatient multidisciplinary
pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
1520
Green RH, Singh SJ, Williams J, Morgan MDL. A randomised controlled trial of four weeks versus seven weeks
of pulmonary rehabilitation in chronic obstructive pulmonary disease. Thorax 2001; 56:143-145
1521
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1522
Williams JEA, Singh SJ, Sewell L, Morgan MDL. Health status measurement: sensitivity of the self-reported
Chronic Respiratory Questionnaire (CRQ-SR) in pulmonary rehabilitation. Thorax 2003; 58:515-518
1523
Hyland ME. The living with asthma questionnaire. Respir Med 1991; 85:13-16
1524
Carone M, Bertolotti G, Anchisi F, Zotti AM, et al on behalf of the Quality of Life in Chronic Respiratory Failure
Group. Analysis of factors that characterize health impairment in patients with chronic respiratory failure. Eur Respir
J 1999;13:1293-1300
1525
Lareau SC, Meek PM, Roos PJ. Development and testing of the modified version of the Pulmonary Functional
Status and Dyspnea Questionnaire (PFSDQ-M). Heart Lung 1998; 27:159-168
181
validity, stability and reliability of both the dyspnoea and the changes in functional ability domains1526.
Changes in dyspnoea do not appear to match declines in lung function over time. Dyspnoea with activities
requiring arm elevation showed a positive relationship with rate of FEV1 decline.
This may be a useful research tool, though no data on its responsiveness to change following interventions
has been found. It appears rather complex and time-consuming for routine clinical practice.
Pulmonary Functional Status Scale (PFSS)1527
This instrument was designed to give strong emphasis to the psychological impact on functional capacity
to perform tasks and allows for tasks not undertaken because of non-pulmonary reasons. It also suits the
older population affected by COPD. It is a self-report questionnaire, which has been refined from 64 items
to 35, with several patterns of response required. It takes around 20 minutes to complete, and yields three
main factors - daily activities/social functioning, psychological functioning, and sexual functioning. Its
total score correlates well with SIP, 12-minute walk test and the psychological functioning subscale. It has
been well-validated, and is said to be responsive to intervention1528.
Quality of Life Index (QLI) - Pulmonary Version III1529
The QLI-III is designed for use in patients with COPD. It is a self-administered 70-item questionnaire that
takes around 10 to 15 minutes to complete, and covers the dimensions of health and functioning,
psychological/spiritual, social and economic, and family. It has been studied in a variety of populations,
and has been shown to be sensitive and responsive to cardiopulmonary rehabilitation1530,1531.
St George Respiratory Questionnaire (SGRQ)
This measure was described in 19921532, and has been extensively validated in several languages. It has
become widely used in bronchodilator and other medication studies in COPD. There are 50 questions, with
76 responses, and takes about 15 minutes for self-completion.
The SGRQ has four dimensions: Symptoms (frequency and severity), Activity, and Impact (social
functioning, psychological disturbances). With weighting of responses there is some difficulty with
scoring, though computerised versions have recently become available (including one developed at the
Prince of Wales Hospital, Sydney). A total score is calculated by combining the three dimension scores
(total score - 0 to 100%, with 100% being maximal disability).
The SGRQ is reliable, reproducible, sensitive to change over time, responsive to interventions1533, and can
be used in both COPD and Asthma1534. SGRQ total scores correlate well with SIP (r=0.65, n=41) and
HADS Anxiety (r=0.50), and SGRQ total score and both Symptoms and Impacts (but not Activity) were
1526
Lareau SC, Meek PM, Press D, et al. Dyspnea in patients with chronic obstructive pulmonary disease: Does
dyspnea worsen longitudinally in the presence of declining lung function? Heart Lung 1999; 28:65-73
1527
Weaver TE, Narsavage GL, Builfoyle MJ. The development and psychometric evaluation of the Pulmonary
Functional Status Scale: an instrument to assess functional status in pulmonary disease. J Cardiopulm Rehabil 1998;
18:105-111
1528
Votto J, Bowen J, Scalise P, et al. Short-stay comprehensive inpatient pulmonary rehabilitation for advanced
chronic obstructive pulmonary disease. Arch Phys Med Rehabil 1996; 77:1115-1118
1529
Ferrans C, Powers, M. Psychometric assessment of the Quality of Life Index. Res Nurs Health 1992; 15:29-38
1530
McEntee DJ, Badenhop DT. Quality of life comparisons: Gender and population differences in cardiopulmonary
rehabilitation. Heart Lung 2000; 29:340-347
1531
Scherer Y, Janelli L, Schmieder L. The effects of a pulmonary education program on quality of life in patients
with chronic obstructive pulmonary disease. Rehabil Nurs Res 1994; 3:62-68
1532
Jones PW, Quirk FH, Baveystock CM, Littlejohn P. A self-complete measure of health status for chronic airflow
limitation. Am Rev Respir Dis 1992; 145:1321-1327
1533
Jones PW, Bosch TK. Quality of life changes in COPD patients treated with salmeterol. Am J Respir Crit Care
Med 1997; 155:1283-1289
1534
Lahdensuo A, Haahtela T, Herrala J, Kava T, et al. Randomised comparison of guided self management and
traditional treatment of asthma over one year. Br Med J 1996; 312:748-752
182
significant covariates with severity of hypoxaemia (p<0.002)1535. Total SGRQ correlates with VO2max in
mild COPD (but not moderate or severe), with r = -0.671536. Distinct differences have been shown between
grades of COPD severity as measured by MRC Dyspnoea Grade1537. Activity in SGRQ reflects the same
factor as MRC Dyspnoea, BDI, OCD, and Dyspnoea in CRDQ. Symptoms and Impacts appear to be
distinct entities, with Symptoms reflecting the same factor as CRDQ Fatigue, Emotional Function and
Mastery. As an outcome measure the SGRQ performs variably. There were non-significant changes seen
in total SGRQ and its three dimensions in the prospective uncontrolled trial of PR1538. The MCID for total
SGRQ score following intervention is currently considered to be 4 units1539.
Seattle Obstructive Lung Disease Questionnaire (SOLQ)1540
This was designed to be self-completed, and to be computer scannable. It was modelled on the CRDQ,
then evolved to a 29-item tool that was validated against CRDQ, CSES satisfaction and physiology
measures. There are three dimensions of health and one of treatment satisfaction. The physical function
scale was loosely based on SF-36, and assesses degree of dyspnoea and the extent of physical limitation.
The coping scale reflects self-efficacy. The other health scale is emotional function, reflecting the impact
of the respiratory condition on psychological well being. It is reliable, valid and responsive, and is simple
to use and to score. It takes most patients 5 to 10 minutes.
1535
Okubadejo AA, Jones PW, Wedzicha JA. Quality of life in patients with chronic obstructive pulmonary disease
and severe hypoxaemia. Thorax 1996; 51:44-47
1536
Hajiro T, Nishimura K, Tsukino M, et al. Stages of disease severity and factors that affect the health status of
patients with chronic obstructive pulmonary disease. Respir Med 2000; 94:841-846
1537
Bestall JC, Paul EA, Garrod R, Garnham R, et al. Usefulness of the Medical Research Council (MRC) dyspnoea
scale as a measure of disability in patients with chronic obstructive pulmonary disease. Thorax 1999; 54:581-586
1538
de Torres JP, Pinto-Plata V, Ingenito E, Bagley P, et al. Power of outcome measurements to detect clinically
significant changes in pulmonary rehabilitation of patients with COPD. Chest 2002; 121:1092-1098
1539
Jones PW. Interpreting thresholds for a clinically significant change in health status in asthma and COPD. Eur
Respir J 2002; 19:398-404
1540
Tu S-P, McDonnell MB, Spertus JA, et al. A new self-administered questionnaire to monitor health-related
quality of life in patients with COPD. Chest 1997; 112:614-622
183
184
Table 5.4
Questionnaire
names
Medical Outcomes
Study Short Form
36 (MOS SF-36)
Respiratory
population
COPD, Asthma,
Cystic Fibrosis,
Rhinosinusitus,
Interstitial Lung
Disorders
No. of
items
36
Time to
complete
5 mins
General Health
Questionnaire
(GHQ-60, 30 &
28)
COPD, Asthma
60, 30
and 28
Beck Depression
Inventory (BDI)
COPD, Asthma
21
10 mins
(GHQ60)
5 mins
(GHQ30
&
GHQ28)
5-10
mins
Generic and Psychological Questionnaires
Domains assessed
Physical functioning; role
limitations due to physical
health problems; bodily pain;
social functioning; general
mental health; role limitations
due to emotional problems,
vitality, energy or fatigue;
general health perceptions.
somatic symptoms; anxiety and
insomnia; social dysfunction;
severe depression
Depression
Administration
format
Self or
interviewer
administered
Selfadministered
Selfadministered
Key Features/ Remarks
Key references
Validity and reliability widely tested,
used with many populations, good
discriminatory potency in interstitial
diseases,
In COPD outpatients, floor and ceiling
effects have been noted, questioning
sensitivity to change following
pulmonary rehabilitation
Screening tool to detect psychiatric
disorders among general psychiatric
outpatients and those in the community.
Focuses on 2 areas: inability to carry
out normal functions; appearance of
new distressing phenomena.
Screen for clinically significant
symptoms of depression, utilised with
many populations and in many setting
Ware, Sherbourne1541
Stewart1542.
Benzo1543.
Boueri1544.
Mahler, Mackowiak1545.
Prieto1546.
Harper1547.
Berry1548.
Goldberg1549.
Beck1550
1541
Ware JE, and Sherbourne CD. The MOS 36-Item Short Form Health Survey (SF-36). Conceptual framework and item selection. Medical Care 1992; 30:473-483
Stewart AL, et al. Functional status and well-being of patients with chronic conditions. JAMA 1989;262:907-913
1543
Benzo R, Flume PA, Turner D, Tempest M. Effect of pulmonary rehabilitation on quality of life in patients with COPD: the use of SF-36 summary scores as outcomes measures. J
Cardiopulmonary Rehabil. 2000;20:231-234
1544
Boueri FM, Bucher-Bartelson BL, Glenn KA, Make BJ. Quality of life measured with a generic instrument (Short Form-36) improves following pulmonary rehabilitation in patients with COPD.
Chest 2001;119(1):77-84
1545
Mahler DA, Mackowiak JI. Evaluation of the short-form 36-item questionnaire to measure health-related quality of life in patients with COPD. Chest 1995; 107:1585-1589.
1546
Prieto L, Alonso J, Ferrer M, Anoto JM. Are results of the SF-36 health survey and the Nottingham Health Profile similar? A comparison in COPD patients. Quality of Life in COPD Study
Group. J Clin Epidemiol 1997; 50:463-73
1547
Harper R, Brazier J, Waterhouse J, Walters S, et al. Comparison of outcome measures for patients with chronic obstructive pulmonary disease (COPD) in an outpatient setting. Thorax
1997;52:879–87
1548
Berry M, Rejeski W, Adair N, Zaccaro D. Exercise rehabilitation and chronic obstructive pulmonary disease stage. Am J Respir Crit Care Med 1999;160;1248–53
1549
Goldberg P. The detection of psychiatric illness by questionnaire: a technique for the identification and assessment of non-psychotic psychiatric illness. London, New York, Oxford University
Press, 1972 Maudsley Monographs no 21
1550
Beck A: The Beck Depression Inventory. Philadelphia, PA: Center for Cognitive Therapy; 1978
1542
185
Questionnaire
names
Hospital Anxiety
and Depression
Scale (HADS)
Respiratory
population
COPD, Asthma
No. of
items
14 items
Time to
complete
5-10
mins
Domains assessed
Centre for
Epidemiological
Studies –
Depression Mode
Scale (CES-D)
Multi-dimensional
Health Locus of
Control
(MHLOC)
Nottingham
Health Profile
COPD
20
5-10
mins
Depression
Selfadministered
COPD, Asthma
18
5 mins
COPD, Cystic
Fibrosis
38
5-10
mins
Profile of Mood
States (POMS)
COPD, Asthma
65
5 mins
Symptom
Checklist 90
Revised (SCL-90R)
COPD, Asthma
90
15
minutes
internality; chance externality; ;
powerful others externality
(replaced with doctors; and
other people in Form C)
Physical mobility, pain, social
isolation, emotional reactions,
energy, sleep
Tension-anxiety, depressiondejection, anger-hostility,
vigour-activity, fatigue-inertia,
confusion-bewilderment.
9 Primary Symptom
Dimensions
3 Global Indices
Anxiety, Depression
Administration
format
Selfadministered
Key Features/ Remarks
Key references
Screen for clinically significant
symptoms of anxiety and depression,
utilised in many populations and
settings
Useful because items place less
emphasis on somatic symptoms of
depression, utilised in many
populations and settings
.Zigmond, Snaith1551
Bjelland1552
Selfadministered
Form C is condition specific
Wallston 19941554
Wallston 19781555
Self or
interviewer
administered
Selfadministered
Reliability and validity tested widely,
responsiveness to interventions for
COPD not clearly established
Reliability and validity tested widely,
utilised in many populations and
settings
Hunt1556
Prieto1557
Selfadministered
Reliability and validity tested in many
populations and settings. Screens for a
range of psychological problems and
symptoms of psychopathology.
Useful as a progress or outcomes
measurement instrument.
Radloff1553
McNair1558
Derogatis1559
1551
Zigmond AS, Snaith RP. The hospital anxiety and depression scale. Acta Psychiatr Scand 1983;67:361–70
Bjelland I, Dahl AA, Haug TT, Neckelmann D. The validity of the Hospital Anxiety and Depression Scale. An updated literature review. J Psychosom Res. 2002 Feb;52(2):69-77
1553
Radloff L. A self-report depression scale for research in the general population. Applied Psychological Measurement, 1977, 1, p.385-401
1554
Wallston KA, Stein MJ, Smith CA. Form C of the MHLC Scales: A condition-specific measure of locus of control. J Personality Assess 1994; 63:534-553.
1555
Wallston KA Wallston BS, et al. Development of the Multidimensional Health Locus of Control (MHLC) scales. Health Educ Mono 1978; 6:160-170
1556
Hunt SM, McEwen J, McKenna SP. Measuring health stats: a new tool for clinicians and epidemiologists. J Royal Coll Gen Pract 1985; 35:185-188.
1557
Prieto L, Alonso J, Ferrer M, Anoto JM. Are results of the SF-36 health survey and the Nottingham Health Profile similar? A comparison in COPD patients. Quality of Life in COPD Study
Group. J Clin Epidemiol 1997;50 (4): 463-73
1558
McNair D, Lorr M, Droppleman L. (1971). Profile of Mood States. Educational and Industrial Testing Service, San Diego, CA
1559
Derogatis LR. (1983). SCL-90-R: Administration, scoring, & procedures manual for the revised version. Baltimore: Clinical Psychometric Research
1552
186
Questionnaire
names
State-Trait
Anxiety Inventory
(STAI)
Respiratory
population
COPD, Asthma,
CRF, CF
No. of
items
40
Time to
complete
10
minutes
Domains assessed
Ways of Coping
Questionnaire
COPD, Asthma
66
10
minutes
Minnesota
Multiphasic
Personality
Inventory
(MMPI)-2
COPD, Asthma
567
60-90
minutes
Psychosocial
Adjustment to
Illness Scale
(PAIS)
COPD, Asthma
46
20-25
minutes
confrontive coping,
distancing, self-controlling,
seeking social support,
accepting responsibility,
escape-avoidance, active
problem-solving, positive
reappraisal.
8 Validity Scales; 5 Superlative
Self-Presentation Subscales; 10
Clinical Scales; 31 Clinical
Subscales (Harris-Lingoes and
Social Introversion Subscales)
15 Content Scales; 27 Content
Component Scales; 25
Supplementary Scales; various
special or setting-specific
indices
Health Care Orientation,
Vocational Environment,
Domestic Environment, Sexual
Relationship, Extended Family
Relationship, Social
Environment, Psychological
Distress.
Anxiety proneness (trait) and
current tension/apprehension
(state)
Administration
format
Selfadministered
Selfadministered
Key Features/ Remarks
Key references
Reliability and validity tested widely,
utilised in many populations and
settings, specific versions available for
adults and children
Reliability and validity tested widely,
used in many populations and settings,
useful for assessing behavioural and
coping strategies used by patients in
stressful situations
Spielberger1560
Folkman, Lazarus1561
Selfadministered
Used to measure psychopathology
across a broad range of client settings.
Diagnoses personality syndromes &
psychopathology Reliability and
validity tested widely, utilised in many
populations and settings
MMPI-2 Manual1562
Semi-structured
clinical
interview, selfreport version
available
(PAIS-SR)
Assesses the psychological and social
adjustment of medical patients (and/or
members of their immediate families)
to illness, Reliability and validity tested
widely, utilised in many populations
and settings
Derogatis1563
1560
Spielberger C, Gonsuch R, Luschene R. (1970). Manual for the State-Trait Anxiety Inventory. Mind Garden: Redwood City, CA.
Folkman S, Lazarus RS. Journal of Personality and Social Psychology, 1985, 48, p.150-170.
1562
MMPI-2 Manual for Administration, Scoring, and Interpretation Revised Edition
1563
Derogatis LR. The psychosocial adjustment to illness scale (PAIS). J Psychosom Res 1986;30(1):77-91
1561
187
Questionnaire
names
Sickness Impact
Profile (SIP)
Respiratory
population
COPD, Asthma,
Cystic Fibrosis,
Sarcoidosis,
CRF
No. of
items
136
Time to
complete
20-30
minutes
Quality of WellBeing Scale
(QWB)
COPD, Cystic
Fibrosis
16
12-20
minutes
Geriatric
Depression Scale
COPD, Asthma
30
5
minutes
Domains assessed
Physical: ambulation, mobility,
body care, movement.
Psychosocial: social interaction,
communication, alertness
behaviour, emotional
behaviour; sleep and rest,
eating, home management,
recreation and pastimes,
employment.
Symptoms, mobility, physical
activity, social activity.
Depression
Administration
format
Self or
interviewer
administered
Interviewer
administered
(Structured)
Selfadministered
Key Features/ Remarks
Key references
Described as responsive but some
studies have shown it to be relatively
insensitive to mild or moderate disease
in COPD patients
McSweeny1564.
White1565.
Scores can be translated into economic
evaluation for cost-effectiveness
studies or quality of adjusted life years
(QALYs), no evidence of sensitivity to
change associated with pulmonary
rehabilitation, sensitivity reported with
Cystic Fibrosis interventions
Appropriate for elderly patients
Anderson1566
Chang1567
Guyatt1568
Yesavage1569
Wigal1570
1564
McSweeny AJ, Grant I, Heaton RK, et al. Life quality of patients with chronic obstructive lung disease. Arch Intern Med 1982; 142:473-478.
White RJ, Rudkin ST, Ashley J, Stevens VAJ, et al. Outpatient pulmonary rehabilitation in severe chronic obstructive pulmonary disease. J Royal Col Phys London 1997; 31:541-545.
1566
Anderson JP, Kaplan RM, Berry CC, et al. Interday reliability of function assessment for a health status measure. The quality of well-being scale. Med Care 1989; 27:1076-1083.
1567
Chang JA, Curtis JR, Patrick DL, Raghu G. Assessment of health-related quality of life in patients with interstitial lung disease. Chest 1999; 116:1175-1182.
1568
Guyatt GH, King DR, Feeny DH, et al. Generic and specific measurement of health-related quality of life in a clinical trial of respiratory rehabilitation. J Clin Epidemiol 1999;52:187-92
1569
Yesavage JA, Brink TL, Rose TL, Lum O, et al. Development and validation of a geriatric depression screening scale: a preliminary report. J Psychiatr Res 1982-83, 17: 37-4
1570
Wigal JK, Creer TL, Kotses H. The COPD Self-Efficacy Scale. Chest 1999; 99:1193-1196.
1565
188
Table 5.5
Questionnaire
names
St. George’s
Respiratory
Questionnaire
(SGRQ)
Chronic
Respiratory
Questionnaire
(CRQ)
Respiratory
population
COPD, Asthma
No. of
items
50
Time to
complete
10-15
minutes
COPD, Cystic
Fibrosis,
Asthma
123
15-30
minutes
Quality of Life
Index (QLI) Pulmonary
Version III
COPD
70
10
minutes
Pulmonary
Function Status
and Dyspnea
Questionnaire
(PFSDQ)
COPD
158
15
minutes
Health-related Quality of Life Questionnaires
Domains assessed
Key Features/ Remarks
Key references
Sensitive to change, many languages
available, reliability and validity widely
tested
Jones, 19921571
Jones, 19971572
Lahdensuo, 19961573
Interviewer
administered
Sensitive to change, resource intensive
(not self-administered), reliability and
validity widely tested, many languages
available, a new self-report version
recently developed
health and functioning,
psychological/spiritual, social
and economic, family
Selfadministered
daily activities/ social
functioning, psychological
functioning, sexual functioning
Self
administered
Utilised with many populations and in
many settings, responsive and sensitive
to change in the one study with a
cardiopulmonary rehabilitation
program
Focus on dyspnoea and functional
status, responsive to pulmonary
rehabilitation interventions, validity
and reliability tested, thorough
assessment of dyspnoea
Guyatt, 19871574
Wijkstra, 19941575
Goldstein, 19941576
Griffiths, 20001577
Lacasse, 19971578
Green, 20011579
Ferrans, 19921580
McEntee, 20001581
Scherer, 19941582
Symptoms (frequency &
severity); Activity; Impact
(social functioning,
psychological disturbances)
Dyspnoea, Fatigue, Emotional
Function, Mastery of Disease
Administration
format
Selfadministered
Lareau, 19941583
Lareau, 19981584.
1571
Jones PW, Quirk FH, Baveystock CM, Littlejohn P. A self-complete measure of health status for chronic airflow limitation. Am Rev Respir Dis 1992; 145:1321-1327
Jones PW, Bosh TK. Quality of life changes in COPD patients treated with salmeterol. Am J Respir Crit Care Med 1997;155:1283-1289
1573
Lahdensuo A, Haahtela T, Herrala J, Kava T, et al. Randomised comparison of guided self management and traditional treatment of asthma over one year. Brit Med J 1996;312:748-752
1574
Guyatt GH, Berman LB, Townsend M, et al. A measure of quality of life for clinical trials in chronic lung disease. Thorax 1987; 42:773-778
1575
Wijkstra PJ, Tenvergert EM, VanAltena R, Otten V, et al. Reliability and validity of the Chronic Respiratory Questionnaire (CRQ). Thorax 1994; 49:465-467
1576
Goldstein RS, Gort EH, Stubbing D, et al. Randomised controlled trial of respiratory rehabilitation. Lancet 1994; 344:1394-1397
1577
Griffiths TL, Burr ML, Campbell IA, Lewis-Jenkins V, et al. Results at 1 year of outpatient multidisciplinary pulmonary rehabilitation: a randomised controlled trial. Lancet 2000; 355:362-368
1578
Lacasse Y, Wong E, Guyatt G. A systematic overview of the measurement properties of the Chronic Respiratory Questionnaire. Canad Respir J 1997; 4:131-139
1579
Green RH, Singh SJ, Williams J, Morgan MDL. A randomised controlled trial of four weeks versus seven weeks of pulmonary rehabilitation in chronic obstructive pulmonary disease. Thorax
2001; 56:143-145
1580
Ferrans C, Powers, M. Psychometric assessment of the Quality of Life Index. Res Nurs Health 1992; 15:29-38
1581
McEntee DJ, Badenhop DT. Quality of life comparisons: Gender and population differences in cardiopulmonary rehabilitation. Heart and Lung 2000; 29:340-347
1582
Scherer Y, Janelli L, Schmieder L. The effects of a pulmonary education program on quality of life in patients with chronic obstructive pulmonary disease. Rehabil Nurs Res 1994; 3:62-68
1583
Lareau S, Carrieri-Kohlman V, Janson-Bjerklie S, Roos P: Development and testing of the Pulmonary Functional Status and Dyspnea Questionnaire (PFSDQ). Heart Lung 1994; 23:242-250
1584
Lareau SC, Meek PM, Roos PJ. Development and testing of the modified version of the Pulmonary Functional Status and Dyspnea Questionnaire (PFSDQ-M). Heart Lung 1998; 27:159-168
1572
189
Questionnaire
names
Seattle
Obstructive Lung
Disease (SOLQ)
Respiratory
population
COPD
No. of
items
29
Time to
complete
10
minutes
Living With
Asthma
Questionnaire
(LWAQ)
Asthma
68
20
minutes
Pulmonary
Functional Status
Scale (PFSS)
COPD
161
15-30
minutes
Maugeri
Foundation
Respiratory
Failure
Questionnaire
(MRF28)
CRF, COPD
28
10
minutes
Domains assessed
physical function, emotional
function, coping skills,
treatment satisfaction
social/leisure, sport, sleep,
holidays, work and other
activities, colds, mobility,
effects on others, medication
use, sex, dysphoric states and
attitudes
ADLs: self-care, transportation,
household tasks, grocery
shopping, meal preparation,
daily activities, relationships,
dyspnoea anxiety, depression
daily activity, cognitive
function, emotional status,
invalidity, perception of general
health, respiratory health
Administration
format
Selfadministered
Key Features/ Remarks
Key references
efficiently measures the functional
status impairments specifically due to
COPD, data for stable vs unstable
disease, promising validity, reliability
and responsiveness
Subscales of functional limitation and
distress
Useful for individual patient
management and clinical trials,
responsive but sensitivity unclear
Tu, 19971585
Selfadministered
Focus on dyspnoea and ADLs, not
widely tested, face and concurrent
validity with SIP
Weaver, 19921588
Mercer, 19971589
Votto 19961590
Selfadministered
specifically designed for patients with
chronic respiratory failure, due to
COPD or kyphoscoliosis, either on
LTOT or NIPPV, many languages
available, good discriminatory potency
between different levels of impairment
of CRF patients
Carone 19991591
Selfadministered
Hyland, 19911586
Hyland, 1991a1587
1585
Tu S-P, McDonell MB, Spertus JA, et al. A new self-administered questionnaire to monitor health-related quality of life in patients with COPD. Chest 1997; 112:614-622
Hyland, ME The living with asthma questionnaire: Respir Med 1991; 85 (Suppl B):13-16
1587
Hyland ME, Finnis S, Irvine SH. A scale for assessing quality of life in adult asthma sufferers. J Psychosom Res 1991; 1:99-110
1588
Weaver TE, Narsavage GL: Physiological and psychological variables related to functional status in chronic obstructive pulmonary disease. Nurs Res 1992; 41:286-291
1589
Mercer KJ, Breslin EH, Follette DM, Allen RP, et al. Comparison in functional state (FS) six months after bilateral lung volume reduction surgery (BLVRS) and pulmonary rehabilitation (PR).
Am J Respir Crit Care Med 1997; 155: A456
1590
Votto J, Bowen J, Scalise P, et al. Short-stay comprehensive in-patient pulmonary rehabilitation for advanced chronic obstructive pulmonary disease. Arch Phys Med Rehab 1996; 77:1115-8
1591
Carone M, Bertolotti G, Anchisi F, et al on behalf of the Quality of Life in Chronic Respiratory Failure Group. Analysis of factors that characterize health impairment in patients with chronic
respiratory failure. Eur Respir J 1999;13:1293-1300
1586
190
Questionnaire
names
Airways
Questionnaire
Respiratory
population
COPD
COPD SelfEfficacy Scale
(CSES)
COPD
No. of
items
30
(AQ30)
or 20
(AQ20)
34
Asthma Quality of
Life
Questionnaire
(AQLQ)
Asthma
32
10-15
Asthma Quality of
Life
Questionnaire
(Marks)
Manchester
Respiratory
Activities of Daily
Living
Questionnaire
(MRADL)
Asthma
20
5
minutes
COPD
Time to
complete
3
minutes
Domains assessed
Administration
format
Selfadministered
Key Features/ Remarks
Key references
Many languages available
Barley, 19981592
5-10
minutes
Negative affect, intense
emotional arousal, physical
exertion,
weather/environmental,
behavioural risk factors
Symptoms, emotions, exposure
to environmental stimuli,
activity limitation
Selfadministered
Self-efficacy measured in terms of
confidence to achieve a physical
activity, not a QOL index
Wigal, 19911593
Self or
interviewer
administered
Many languages available, reliability
and validity widely tested,
responsiveness and sensitivity tested,
minimally important difference
developed, widely used
Validity and reliability reported,
developed in Australia
Juniper, 19931594
Juniper, 19921595
Boulet, 19951596
Gibson PG. Talbot PI,
Toneguzzi, 19951597
Marks, 19931598
Marks, 19921599
Breathlessness and physical
restrictions, mood disturbance,
social disruption, concerns for
health
Selfadministered
Composite of questions from the
Nottingham Extended ADL
Questionnaire (NEADL) and Breathing
Problems Questionnaire (BPQ).
Sensitive to PR interventions, useful for
older populations, respiratory specific
ADL index
Yohannes, 20001600
Self or
interviewer
administered
1592
Barley EA, Quirk FH, Jones PW. Asthma health status in clinical practice: validity of a new short and simple instrument. Respir Med 1998; 92:1207-1214
Wigal JK, Creer TL, Kotses H. The COPD Self-Efficacy Scale. Chest 1991; 99:1193-1196
1594
Juniper EF, Guyatt GH, Ferrie PJ, Griffith LE. Measuring quality of life in asthma. Am Rev Respir Dis 1993;127:832-838
1595
Juniper EF, Guyatt GH, Epstein RS, Ferrie PJ, et al. Evaluation of impairment of health-related quality of life in asthma: development of a questionnaire for use in clinical trials. Thorax
1992;47:76-83
1596
Boulet L, Boutin H, Cote J, et al. Evaluation of an asthma self-management education program. J Asthma 1995;32:199-206
1597
Toneguzzi RC, Population Medicine Group 91C. Self-management, autonomy, and quality of life in asthma. Chest 1995;107:1003-1008
1598
Marks GB, Dunn SM, Woolcock AJ. An evaluation of an asthma quality of life questionnaire as a measure of change in adults with asthma. J Clin Epidemiol 1993; 46:1103-1111
1599
Marks GB, Dunn SM, Woolcock AJ. A scale for the measurement of quality of life in adults with asthma. J Clin Epidemiol 1992;45:461-472
1600
Yohannes AM, Roomi J, Winn S, Connolly MJ. The Manchester Respiratory Activities of Daily Living Questionnaire. (Development, Reliability, Validity, and Responsiveness to Pulmonary
Rehabilitation). J Am Geriatr Soc 2000; 48:11
1593
191
Questionnaire
names
Air Index
Respiratory
population
Asthma
No. of
items
63
Time to
complete
15-20
minutes
Breathing
Problems
Questionnaire
(BPQ)
COPD, Asthma
33 (Long
Version),
10 (Short
Version)
3-10
minutes
Domains assessed
Psychological, Physical
Activity, Physical Symptoms,
Social
Walking, Bending or reaching,
Washing and bathing,
Household chores, Social
interactions, Effects of weather
or temperature, Effects of
smells and fumes, Effects of
colds, Sleeping, Medicine,
Dysphoric states, Eating,
Excretion urgency
Also can calculate scores based
on two constructs: health
knowledge and health appraisal
Administration
format
Selfadministered
Selfadministered
Key Features/ Remarks
Key references
Validity and reliability established,
responsiveness and sensitivity not
established
Available in other languages,
responsive to changes following
pulmonary rehabilitation
Letrait, 19961601
Hyland, 19941602
Hyland, 19981603
1601
Letrait M, Lurie A, Bean K, Mesbah M, Venot A, Strauch G, et al. The Asthma Impact Record (AIR) Index: a rating scale to evaluate the quality of life of asthmatic patients in asthma. Eur Respir
J 1996; 9:1167–73
1602
Hyland ME, Bott J, Singh S, Kenyon CAP. Domains, constructs, and the development of the breathing problems questionnaire. Qual Life Res 1994; 3:245-256
1603
Hyland ME, Singh SJ, Sodergren SC, Morgan MDL. Development of a shortened version of the Breathing Problems Questionnaire suitable for use in a pulmonary rehabilitation clinic: a purposespecific, disease-specific questionnaire. Qual Life Res 1998; 7:227-233
192
193
APPENDIX 1
Pulmonary rehabilitation programs in
Australia
A.1.1.
ALF Better Breathing Program
Survey of Patient Perspectives of Pulmonary
Rehabilitation
The Australian Lung Foundation commissioned an evaluation in 1999 of patient perspectives of
Pulmonary Rehabilitation (PR) in an attempt to identify the critical factors for success, the "core
elements" required, and current referral systems.
The evaluation had an initial small-scale qualitative phase, which was followed by a more
comprehensive quantitative phase. The former comprised face-to-face interviews with patients in
their homes. Eight patients who had been in three different programs were interviewed in March
2000. The sample covered patients who completed a PR program and joined a patient support
group (PSG), patients who only completed a PR program and did not join a PSG, and patients
who did not complete their full PR program. From the responses a range of questions were
developed for the quantitative phase.
Description of quantitative survey
The structured questionnaire for telephone interviews was piloted before being used in the active
quantitative survey. Interviews were conducted by phone over an average time of 40 minutes.
There were 151 interviews conducted, over May and June 2000. The patients interviewed were
selected by ballot from patient lists provided by hospitals and program volunteers. They covered
a wide span of ages, and they represented 24 PR programs across different cities, regional and
rural as well as urban. As in the earlier phase, patients selected represented those completing PR
and joining PSGs (46%), those completing PR but not joining PSGs (44%), and those who did
not complete PR (9%). The structured interviews were coded for a range of patient
characteristics, location of program, program characteristics, patient expectations and ratings of
program characteristics and outcomes, and issues about PSGs. These data were computer
processed along with patient psychographic measures, and analysed.
Patient characteristics
Two-thirds of programs were city-based. State-distribution of patients were: 30% New South
Wales, 21% each Victoria and South Australia, 12% Western Australia, 10% Queensland, and
7% Tasmania. The gender ratio was 59% male, 41% female. The majority were aged more than
60 (30-49 = 1%, 50-59 = 13%, 60-69 = 30%, 70-79 = 47%, 80-plus 10%. Respiratory diagnoses
coded included emphysema (75%), asthma (42%), chronic bronchitis (13%), COPD/COAD
(13%), and bronchiectasis (10%). Non-respiratory conditions were also often coded - especially
arthritis (41%), hypertension (25%) and osteoporosis (23%). Most patients (92%) did not attend
with a carer or family member, and 40% actually lived alone. The majority appeared to be in
194
mild to moderate disability, as 79% felt comfortable walking outside, and 5% were still in paid
employment. Most (86%) had been smokers in the past, and only 9% had never smoked. Word of
mouth, rather than advertisements, was the most common source of awareness about the
programs (96%), and Specialists were the most usual source of referral (49%). For the 17 patients
who did not attend all sessions and the 14 who dropped out of their program, sickness was the
most common limiting factor.
Expectations and Perceived outcomes
Most participants expected improvements in breathing (30%) and exercise capacity (21%), but
there was a range of other expectations. Overall program ratings averaged between highly
beneficial (32%) and extremely beneficial (54%), though 4% rated their program as "not at all
beneficial". Perceived benefits were related to achievement of or exceeding expectations in
exercises, breathlessness and fitness. Low ratings of benefit came especially from the oldest
clients and from respondents who did not complete the program. Some felt they were pushed too
hard, while others felt they did not reach their expectations of gain in fitness. After completion of
the program most patients continued some form of exercise, mostly walking (82%), while a
minority used gym equipment (33%) and/or weights (1%), predominantly at home (89%). Almost
60% felt their fitness was greater after the program than before, although respiratory problems
had interfered with exercise in almost half the survey respondents. Knowledge and awareness
were perceived as slightly more beneficial than fitness and general wellbeing, yet rather
paradoxically, in programs offering the greatest amounts of formal education the perceived longterm fitness subsequently was less. The information deemed to be of greatest interest/benefit
covered use of medications (41%), breathing techniques (35%), physical exercise (30%) and
nutrition (25%), though there was substantial variance across programs, probably depending on
the emphasis and available personnel.
Access
Most respondents (82%) had no access difficulties, though it must be acknowledged that poor
access would have a selection bias. Distance from the program and parking were the most
prevalent access complaints. Most (81%) had to travel less than 30 minutes to attend, but city
respondents and women reported longer travelling times. Most travelled by car (75%), especially
in regional and rural areas, though women were more likely to travel by public transport. Most
patients (83%) waited less than 3 months to start their PR participation.
Course characteristics
Physiotherapists coordinated 56% of programs, and 29% were run by respiratory nurses. There
was a high degree of satisfaction with program coordinators. Most courses lasted from 6 to 8
weeks, and most participants attended only one session per week (57%). Group sizes ranged from
a few as 4 to as many as 30 (median = 10). Socialisation occurred in two-thirds of programs, and
most (75%) patients felt this was important time for them. Most patients (88%) received reference
material while in the program, and 95% of those receiving such material found it useful,
especially to refer to later. Sessions were usually 90 to 120 minutes (61%), and most (89%)
included exercise. When exercise training was included there was a high participation rate in the
exercises (88%), and the sessions were most likely to be an hour or more (58%). Those patients
attending exercise training perceived greater long-term benefit, and those attending for longer
times gained greater enjoyment and perceived greater fitness gains. A variety of exercises was
employed, with gym equipment and weights being commonly utilised (88% each). Most
participants also did exercises at home during the program (79%), almost half on at least 6
occasions per week (49%), 30% of them for more than 30 minutes.
195
Follow-up and Patient Support Groups
Follow-up contact between patient and program staff was common (68%), especially in those
joining PSGs (84%), and especially males (75%). This contact was highly valued, although those
who did not have follow-up contact actually preferred it that way. Three-quarters of all
participants expressed interest in repeating their program, and 41% remained in PSGs after their
participation in PR. There were many reasons why people wanted to repeat their participation,
and equally many for those not wanting to repeat – however no consistent message was apparent.
PSG membership was not taken up by 58% of respondents, 17% of whom had never heard of
them, 13 % lived too far away, 7% were too busy, while cumulatively 24% had their own support
network, found their doctors provided enough, participated in other service groups, or preferred to
help themselves. PSGs were valued for their capacity to provide social contacts (56% of
respondents), more than for formal lectures (26%) or information updates (11%).
Conclusions
1. 85% rated their PR programs positively.
2. The main benefits related to better breathing, better fitness and greater knowledge of
exercises and breathing techniques.
3. Long-term benefits were often perceived.
4. Benefit did not relate to length or intensity of program.
5. Establishing and extending physical limits appeared to provide confidence to exercise
more at home.
6. Components valued highly were exercise training, formal education, resource materials,
and informal social contacts.
7. A balance needs to be established between education and exercise training inputs.
8. Little emphasis has been put on specific behaviour change strategies.
9. Heterogeneity of disease, severity of disability, program, and group size were not
considered important influencing factors.
10. Follow-up was important especially for those who are less well.
11. Many patients would wish to repeat PR.
12. Continuation exercise was highly valued.
13. Access created difficulties for women in particular.
196
A.1.2.
ALF Better Breathing Program
Survey of Pulmonary Rehabilitation
Programs in Australia
This project was conducted in 2000 under the supervision of Sue Jenkins (physiotherapist
coordinator of a PR program) for the ALF. Submissions from organisations and individuals on an
ALF register (PR Network) were invited. Fifty-three Australian PR programs were identified as
being current, and a representative from each was surveyed by structured telephone interview.
Another 14 had made submissions previously but their funding had failed, or they were still in a
set-up phase. Of the fifty-three, 38 were based in major teaching hospitals, regional base
hospitals, or smaller private hospitals, and 15 were run from community centres. All states were
represented: Victoria (12), New South Wales (11), Queensland (9), Western Australia (9), South
Australia (6), Tasmania (4) and Australian Capital Territory (2). A range of characteristics was
surveyed, from referral patterns, through personnel involved, program components, assessment
tools, outcome measures and follow-up.
Patient throughput
Nationally 2,554 patients completed PR in 1999. Six programs reported throughputs of over 100
patients in the year, while the median number per site per year was 35. Most patients had COPD,
though the proportion with COPD ranged from 30% to 100% (median 85%). Thirty-two
programs catered for pre and post surgical candidates (LVRS and transplantation). Most
programs included carers, and over two-thirds (68%) provided some form of maintenance
sessions. Half the programs had waiting lists, from 2 to 7 months.
Referral patterns, and links with GPs
Most referrals were from respiratory specialists (83%), GPs (71%) and thoracic surgeons (67%).
Twenty-two percent of programs accepted self-referrals. Strong links with GPs were reported
from 9 centres (including two linked to coordinated care programs), but the majority reported
weak (39) or non-existent (5) links to GPs. Hospital inpatients (32%) and physiotherapists (28%)
were important referral sources. Only 7.5% had referrals from patient support groups.
Program components
Four programs provided only education sessions, while 11 provided only exercise training
(though two of these also provided information on smoking, infections, stress management and
community resources). The remaining 38 provided education and exercise. In the 42 programs
providing education, a wide range of topics was offered. Most commonly this related to exercise
(90.5%), breathing exercises (90.5%), and activities of daily living and energy conservation
(73.5%). Stress management and coping were addressed by 83%, relaxation was taught in 64%,
and psychological issues were addressed by 69.8%. Information was provided about medications
by 81%, inhalation devices by 75.5%, prevention of infections by 60%, oxygen therapy by
58.4%, and community resources by 71.6%. Smoking was specifically addressed in only 49%,
while information about lung function (52.8%), nutrition (81%), and support groups (58.5%)
were more often programmed. Incontinence (26%) and sexuality/relationships (16.9%) were
uncommon components. Carer issues were addressed by 49% of programs.
197
Staffing
Most programs (72%) were coordinated by physiotherapists, while 24.5% were coordinated by
nurses. One occupational therapist and one psychologist were listed as coordinators. Patient
information sessions were provided by physiotherapists in all but one program and by nurses by
62%. Occupational therapists (75.4%), dieticians (73.5%), pharmacists (66%), and social workers
(62%) were highly represented presenters. Other contributors were psychologists (30%), mental
health nurses (11%), respiratory scientists/technicians (16.9%), respiratory physicians (41.5%)
and GPs (13.2%).
Assessments
Patients underwent formal assessments in all programs, all but four recording a medical history
and well under half recording lung function (40%). Some form of exercise performance
assessment was made in 87% (the most common was a 6-minute walk test). At least one form of
quality of life assessment was made in 60% (the disease-specific Chronic Respiratory
Questionnaire in 32% and St George’s Respiratory Questionnaire in 26.4%, and the generic SF36
in 8%). No programs recorded measurement of specific psychological measures, though selfefficacy, locus of control or self-esteem were assessed in two. Health care utilization indexes
(hospitalization etc) were recorded routinely by only one program.
Post-program assessments were undertaken in all 53 programs. The outcome measures were:
exercise performance (85%), quality of life (55%), lung function (38%), and patient satisfaction
(13%).
Follow-up
Some form of follow-up monitoring assessment was made at 3 months by 32% of programs, at 6
months by 56.6%, at 9 months by 15%, and at 12 months by 35.8%. Referrals were made to
patient support groups from 90.5% of the 53 PR programs.
Conclusions
1. People with moderately severe and severe COPD represented the main clientele of PR
programs in Australia in 1999.
2. A small minority (less than 1%) of the estimated half-million Australians with
symptomatic COPD are able to access current programs.
3. The most common sources of referrals in 1999 were respiratory physicians and GPs,
though links to GPs were considered very weak.
4. Most programs provided both education and exercise training, with a high level of
attention reported to stress management as well as breathing exercises.
5. Areas of specific information deficiency were continence and sexuality, and smoking.
6. Only half of the programs addressed carer issues specifically, despite most encouraging
carers to attend.
7. Physiotherapists and nurses were highly represented as information providers, with
doctors, mental health workers and pharmacists being less frequently involved.
8. Lung function was not widely used as an initial assessment tool (or outcome measure).
9. Exercise performance was almost universally assessed initially and as an outcome, most
often with a 6-minute walk test.
10. Quality of life was measured in only 40% of programs (disease-specific the most usual),
and psychological measures were rarely assessed.
11. Eighteen of the 53 programs did not have any follow-up visits programmed, although all
but one of these recommended or referred patients to support groups.
198
A.1.3.
ALF Patients Needs Analysis
A Patient Needs Analysis was undertaken in 1999 by Pieter Walker (respiratory psychologist) for
the ALF, utilising both questionnaires and focus groups with structured discussion and analysis.
Patients who were members of LungNet Patient Support Groups were invited to participate.
Patient demographics
There were 576 respondents, with an average age of 66.6 years, and a male : female ratio of 53%
to 47%. There was a representative mix of diagnoses – 56% emphysema, 37% asthma, 22%
bronchitis, and 37% “other respiratory diagnoses”. Over 70% had a smoking history. Patients
were on average severely disabled, with 86.4% of them perceiving their condition as at least
moderately severe, 41% of them were using long term oxygen therapy, and almost half had been
admitted to hospital at least once in the past year. The average number of respiratory medications
used by them was 3.5.
Impacts on Quality of Life
Questionnaire analysis showed functional status was the main contribution to poor quality of life.
This included limits to leisure activities, physical mobility and household activities. Other factors
contributing to poor quality of life included (in order) lack of knowledge, poor community
awareness and understanding of lung diseases, costs of their illness (medications, visits to health
professionals, and foregone employment), poor communication from their doctors, and social
stigma and isolation. In the focus groups, psychological impacts such as anxiety, depression and
low self-esteem were identified as the most significant factors in poor quality of life.
Services and Information
The most frequently accesses health services were (in order) GPs, pharmacy, support group and
respiratory physician. There was a high level of satisfaction with GP care, though patients
recognized that GPs needed better training about chronic lung disease management, and about
communication with patients. Focus groups rated support groups and rehabilitation highly, but
reported that access to rehabilitation and counseling was currently inadequate. They also felt
more information about support services, diseases and medications was required. Services such as
district nursing, domiciliary care and meals on wheels were under-utilised. Further, access to and
availability of medications, and inadequacy of medication information (especially drug side
effects) were identified as problematic. Of the information they received, 76% came through
respiratory specialists and 74% through GPs or other doctors, most commonly verbally (87%).
Only 47% recalled receiving printed information, and there was essentially no use of audio-visual
or computer educational aids reported.
Conclusions
1.
2.
3.
4.
Quality of life was adversely affected by psychological factors.
However, access to counseling, rehabilitation and other support services was sub-optimal.
Patients want better access to clear information about medications and their side effects.
An independent central resource (ALF) for information about disease management was
highly valued, above pharmaceutical company patient information.
5. Telephone counseling and help-line services were reported as highly desirable.
6. Self-management aids, client-held records, and action plans were considered important.
199
A,1.4.
Pulmonary Rehabilitation Survey,
2007
A Market Research Survey was undertaken for ALF by StollzNow, and reported in July 2007. A
total of 137 PR coordinators completed questionnaires, in 96% of cases at a time when a PR
program was in existence on site. The survey covered rural and metropolitan areas, in all states
and territories. Several main themes were addressed.
Program Aspects
71% of programs were conducted as regular group courses over a specific time-frame, with 27%
running as continuous �rolling’ programs.
Course characteristics
9
9
9
9
The national average for participants attending is 1.8 times per week
The national average for duration is 9 weeks
The national average number of participants is 8.4 per group
Referral sources are mostly specialists (43.7%), with primary care is the source for
33.9%
9 There are specific entry criteria for 45% of programs, mostly applying diagnostic
groups (86%), but in 33% severity is a lead criterion
Waiting lists
9 The national average for patients on a waiting list is 13.5 patients
9 17% of programs have waiting times �more than 8 weeks’
9 the national averaging waiting time to enter a program is 5.9 weeks beyond the start
of the next program
Challenges and Barriers
52% of programs identified a variety of challenges, mainly related to patient transport (56%),
patient drop-out (51%) and uncertain funding (47%).
Other important challenges were staff attraction and retention (37%), lack of support from the
hospital (35%) and adequacy of referrals (21%).
96% were sure there are patients not attending who could gain benefits by being referred.
Funding sources
Of the many identified funding sources, �within hospital funding’ was the most common (51%),
followed by specific �state funding’ (35%).
Barriers to attendance
9
9
9
9
9
9
lack of awareness by primary care (74% - 84% in rural areas)
transport difficulties (65% - 56% in rural areas)
lack of acceptance by patients (52%)
lack of awareness among specialists (40%)
lack of funding (38%)
lack of parking(37% - 29% in rural areas)
Maintenance
82% of PR coordinators indicated they refer their patients for maintenance courses following
completion of the PR course. In 66% these are �commuity based’, though in NSW 62% were
200
based in hospitals. Very few were conducted in a gym or at home. The 18% who did not refer on
were not aware of maintenance programs available in the vicinity.
Support groups and ALF resources
62% of PR coordinators refer patients on to support groups. The remainder were unaware of local
support groups.
Important linkages between programs and the ALF were identified. 70% of programs provided
information about ALF supports during lectures, and 68% provided ALF literature.
There was strong interest in the ALF providing information about PR programs – effective
methods considered were GP posters (76%), hospital posters (74%), letters and information to
primary care (69%) and letters and information to specialists (62%)
Media campaigns were thought to be probably ineffective.
Conclusions
1. PR programs are available in all states and territories (with fewest being available in
ACT). Distribution according to population and geography was not documented.
2. Most courses have twice-weekly attendance, with around 10 patients per group, running
for an average of 9 weeks. These match guidelines satisfactorily
3. Only one-third of programs received GP referrals.
4. On average there are over 10 patients on waiting lists per program, and these patients on
average wait for around 6 weeks after the next group starts (i.e. for up to 13 weeks).
5. Program funding and patient access difficulties are the major challenges in keeping
programs running.
6. Lack of awareness of PR by both GPs and specialists, lack of acceptance by patients of
the role and benefits of PR, and transport difficulties are major barriers for delivering
PR.
7. Maintenance program availability is an important �missing link’ between evidence and
practice.
201
A.1.5.
Comprehensive Pulmonary
Rehabilitation.
A Sample Program
This example should not be seen to be the paragon of Pulmonary Rehabilitation. There are more
extensive details to be found in the ALF/APA Pulmonary Rehabilitation Toolkit, which can be
accessed through http://www.pulmonaryrehab.com.au.
Education Course
A comprehensive education package, including:
Training in partnership self-management
Anatomy and physiology of the lung and lung mechanics
Sputum clearance, bronchial hygiene and breathing techniques
Benefits of exercise
Dealing with stress / anxiety and depression
Respiratory medications (pharmacy)
Use of respiratory devices / and O2
Weight maintenance and good nutrition
Difficult issues (sex, relationships, continence, end-of-life, palliation)
Activities of daily living / task simplification
Social, family and community supports
Experience has suggested:
• Group sizes of 6 to 12 patients work best (with additional significant others).
• Classes are led by a relevant specialist allied health / nursing / medical worker.
• Training classes should encourage full participation of patients and their spouse / carer.
• Therapists should stress the importance of enjoyment and provide leadership on developing
self-confidence to communicate with doctors and other health workers, enabling a capacity to
self-monitor and self-manage.
• The duration of the course depends on local practicalities and the ability of the participants to
attend multiple times. On average 2 hours per week for 8 weeks should cover most aspects.
Exercise Training Program
Participants attend a supervised and monitored exercise program in a gymnasium, involving:
Upper and lower limb training
Focus on improving endurance, muscle strength and flexibility
General exercise program
Interesting activities
Learning how to do it at home
Breathing exercises.
Experience and the medical literature have suggested:
• Participants should perform exercise at least 3 times a week for at least 45 minutes to achieve
training over 6 to 8 weeks.
• Exercise classes are limited to small numbers (less than 15) so that safe, individualised
attention can be given.
202
•
•
•
Where the subject’s pO2 is less than 55mmHg or the SpO2 is less than 87%, supplemental
oxygen is provided and the participant monitored carefully in each early session. This helps
to reassure the therapist, patient and carer about setting safe limits for ongoing exercise.
In addition, participants are encouraged to undertake regular home exercises.
They may be issued with a booklet (containing pictures of the exercise to be done at home),
sometimes a pedometer or similar activity monitor, and a behavioural diary.
Psychosocial Supports
Participants are encouraged to enrol in a patient support group, and they receive advice on the
community network of social programs and supports.
• Through the course, if patients want individual advice, or a therapist identifies a need for such
advice, counseling should be made available.
• Notable areas are anxiety or depression, stress management, sex/relationship counseling,
nutrition advice, terminal care issues, incontinence, etc.
Patient Screening Evaluations
The aims of initial patient assessment are numerous. They include introducing patients to key
staff and facilities and characterising their medical conditions and comorbidities. Specific issues
include determining the severity of the respiratory impairment, degree of reversibility, and
functional performance, documenting what medications are actually taken (and alerting managing
doctors to potential problems), highlighting mobility, nutritional and psychosocial issues that
need to be addressed, and providing baseline reference values for outcome measures.
Demographics
•
•
•
•
•
•
age, race, gender
smoking history (current habit, date of quitting (if relevant), average consumption over
years)
main respiratory diagnoses (eg chronic bronchitis, asthma, emphysema, bronchiectasis,
pulmonary fibrosis) and their duration
use of domiciliary oxygen (dose, duration of use, and date of starting),
other medical conditions currently relevant or contributing to disablement
current medications actually used (and those prescribed), including "adjunct",
"alternative", and "herbal" products.
Carer status
•
•
presence of an immediate carer at home
well-being of the carer
Lung Function
•
•
•
forced expiratory volume in 1 second (FEV1), forced and slow vital capacity (FVC &
SVC) and inspiratory capacity (IC) pre and post bronchodilator (for severity of
respiratory impairment and reversibility)
arterial blood gas analysis (ABG) for PaO2 and PaCO2 (for degree of hypoxaemia, and
presence of acute or chronic respiratory failure)
static lung volumes and gas transfer factor (for degree of hyperinflation and gas transfer
impairment)
203
•
functional exercise capacity with perceived distress (eg Borg for fatigue and dyspnoea)
and oximetry
Psychology
•
•
•
•
Overall psychological health (eg GHQ28)
Specific psychiatric diagnoses (eg HADS)
Cognitive status (eg MMS)
Mood disturbance (eg POMS)
A report of findings should be provided for referring practitioners and other health workers
involved in the patient's care.
Primary Outcome measures
•
•
•
•
Functional exercise capacity (eg 6-minute walk test or endurance shuttle walk test)
HRQoL Questionnaires (eg SGRQ, CDQ, SF36)
Other focussed questionnaires (eg coping, self-efficacy, etc)
Health care utilisation (eg number of hospital attendances, length of stay in hospital
admissions, programmed and urgent visits to GPs and specialists, actual out-of-pocket
expenditure by patient and carer)
A report of progress following the main program should be provided for referring practitioners
and other health workers involved in the patient's care.
204
APPENDIX 3
Submissions to ALF
The Australian Lung Foundation sponsored the preparation of this document, and as part of that
sponsorship invited expressions of interest in developing Standards for PR from all organisations
and individuals on their PR Network database in December 2001. Submissions were received
from the following:
AUSTRALIAN PHYSIOTHERAPY ASSOCIATION. The National Cardiothoracic Special
Group of the Australian Physiotherapy Association, written by Dr Marie Williams, Chairperson,
and Ms Kathy Mecca, Victoria Representative, National Cardiothoracic Special Group,
Australian Physiotherapy Association.
THE ALFRED HOSPITAL MELBOURNE. Prue Munro, Senior Clinician Physiotherapist, Lung
Transplantation Unit; and Anne Holland, Senior Physiotherapist, Pulmonary Rehabilitation
Program, The Alfred Hospital, Melbourne, VIC
AUSTIN & REPATRIATION MEDICAL CENTRE MELBOURNE. Catherine Hill, Senior
Physiotherapist, Pulmonary Rehabilitation, Austin & Repatriation Medical Centre, Prahran, VIC
ROYAL BRISBANE HOSPITAL PERTH. Cherie Hearn, Senior Physiotherapist, LATTICE
team, Royal Brisbane Hospital, QLD
CONCORD HOSPITAL SYDNEY. Andreas Heidemann, Pulmonary Rehabilitation, C 31
Respiratory Unit, Concord Hospital, NSW
PRINCESS MARGARET HOSPITAL FOR CHILDREN PERTH. Kylie Johnstone, PhD student,
Curtin University of Technology, Clinical Specialist Physiotherapist (Cardiopulmonary), Princess
Margaret Hospital for Children, Perth, WA
MID NORTH COAST AREA NSW. Kempsey District Hospital and the Mid North Coast Area
Health Service, NSW. Chris Hanna, Project Officer, Priority Health Care Programme, Health
Service Development Unit, Port Macquarie Health Centre, Port Macquarie, NSW
PRINCE OF WALES HOSPITAL SYDNEY. Cynthia Ashley, Health Professional involved with
PR Programs, Prince of Wales Hospital, Randwick, Sydney, NSW
PRINCE OF WALES HOSPITAL SYDNEY. Health Professional involved with Pulmonary
Rehabilitation Programs, Discipline: Speech Pathology. Submitted by Sally White, Senior
Speech Pathologist, Rehabilitation and Aged Care, Prince of Wales Hospital, Randwick, NSW
ROYAL PERTH HOSPITAL. PERTH. Kylie Hill, (Senior respiratory physiotherapist) and Peta
Winship (Senior cardiothoracic physiotherapist), Royal Perth Hospital, WA
ROYAL PRINCE ALFRED HOSPITAL SYDNEY. Pulmonary Rehabilitation Unit, Department
of Physiotherapy, Royal Prince Alfred Hospital, Submitted by Jenny Alison and Lissa Spencer,
Sydney, NSW.
205
SHOALHAVEN REGION. Submitted by Tod Adams, CNC Chronic and Complex Care, CVA
& CAL Coordinator, Nowra, NSW
ST VINCENTS HOSPITAL MELBOURNE. Pulmonary Rehabilitation Coordinator, Amanda
Kochevatkin, Senior Physiotherapist, St Vincents Hospital, Melbourne, VIC
WHITEHORSE COMMUNITY HEALTH SERVICE VIC. WCHS Pulmonary Rehabilitation
Program (PRP), Edward Chan (physiotherapist) and Olive Aumann (community health nurse)
with input from participants (and their carers) and the Whitehorse Respiratory Support Group;
from the Whitehorse Community Health Service, Box Hill, VIC.
THE NORTHERN HOSPITAL MELBOURNE. David Berlowitz, PhD student (Physiotherapy),
University of Melbourne, and Coordinator, Cardiovascular and Respiratory Medicine Research
Program, The Northern Hospital, Melbourne, VIC.
SIR CHARLES GAIRDNER HOSPITAL PERTH. Dr Sue Jenkins and Nola Cecins, Pulmonary
Rehabilitation Physiotherapists, Physiotherapy Department, Sir Charles Gairdner Hospital,
Nedlands, WA 6009
THE WESLEY HOSPITAL BRISBANE. The Introduction of a Pulmonary Rehabilitation
Program, Submitted by Elizabeth Egan, The Wesley Hospital, Brisbane, QLD
EPWORTH HOSPITAL MELBOURNE. Caroline Nicolson, Physiotherapist, (including
Business Plan and Audit Results), Epworth Hospital, Bridge Road, Richmond VIC
Pulmonary Rehabilitation at Grace McKellar Centre. Submitted by Bonita Emsley, Pulmonary
Coordinator, North Geelong Community Rehabilitation Centre, Barwon Health, Ballarat Road,
North Geelong, VIC
GREENSLOPES PRIVATE HOSPITAL BRISBANE. Respiratory Rehabilitation at Greenslopes
Private Hospital, submitted by L Molloy, Program Coordinator, Brisbane, QLD
REPATRIATION GENERAL HOSPITAL ADELAIDE. Pulmonary Rehabilitation Annual
Report, Peter Frith, Department of Respiratory Medicine, Repatriation General Hospital, Daw
Park, SA
�Personal Expressions of Interest’
Dr John Booth, Exercise Physiologist, Wollongong, NSW
Ms Vicki Neale, Post-Lung Transplant patient, South Plymptom, SA
Consumer at Royal Prince Alfred Hospital Pulmonary Rehabilitation program, by Virginia
Northwood, President, LAM Australia Inc, LEICHHARDT, NSW
Research and Development Papers
Preliminary outcome of COAD Rehabilitation, Submitted by Maria Podger, Ipswich Hospital,
QLD
206
EVALUATION OF AN OUTPATIENT PULMONARY REHABILITATION PROGRAMME.
Submitted by Vanessa McDonald, Clinical Nurse Consultant, Respiratory Medicine, John Hunter
Hospital, Newcastle, NSW
Evaluation & Progress Report of Programmes for Chronic Airways Limitations Disease, May to
July 2001. Manning Base Hospital, Mid North Coast Area Health Service. By Karyn Jarvie, Port
Macquarie, NSW
Grant Submission for "Breathing Easier in East Gippsland - An Evidence Based Pulmonary
Rehabilitation Program", from Chris Shoemaker, Bairnsdale Regional Health Service, VIC
"Clinical Pharmacy Input into a Respiratory Rehabilitation Program." Aust J Hosp Pharm 1998;
28:181-184, submitted by Christopher Alderman, Chief Pharmacist, Repatriation General
Hospital, Adelaide, SA
a) Australian surveys and guidelines
I
Best Practice Guidelines for Cardiac Rehabilitation, Victoria
II
NSW Policy Standards for Cardiac Rehabilitation
III
Literature Systematic Review since 1995 (Cranston, Crockett, Frith 2001,
Cafarella, Duffy, Frith 2005-8)
IV
COPD Case Statement, ALF 2000
V
Australian and New Zealand Guidelines for Diagnosis and Management of
Chronic Obstructive Pulmonary Disease (2003 and updated 2006)
b) International surveys and guidelines
I
American Pulmonary Rehabilitation Guidelines 1995
II
ERS Task Force Position Paper 1997
III
BTS Statement on Pulmonary Rehabilitation 2001
IV
Other Systematic Reviews (eg Lacasse et al 1997, 2003)
V
GOLD Workshop Report and Executive Summary (2001 and updates to 2006)
1.1. Regional physiotherapy (Veronica Brydon)
1.2. Bankstown Hospital (Regina Leung)
1.3. Queensland COPD Interest Group
1.4. Western Hospital Melbourne Research Proposal
1.5. Perth/Adelaide Health Economics Research Proposal
207
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