clinical practice guidelines for physical therapy in ... · on the basis of history-taking,...

1

KNGF-guidelines for physical therapy in patients with chronic obstructive pulmonary disease

V-03/2003/US

IntroductionThese guidelines concern the diagnosistic and

therapyeutic processes involved in providing physical

therapy for patients with chronic obstructive

pulmonary disease (COPD). The decisions made in

arriving at Justification of the guideline

recommendations are described in detail in the

second part of these guidelines, which is entitled

“Review of evidence”.

Target group

These guidelines are intended for physical therapists

who treat patients who, as a result ofbecause of COPD,

have impaired mucus clearance, whose normal daily

life activities are limited by dyspnea, or who have

impaired exercise capacity. These physical therapists

are expected to have the relevant expertise and the

diagnostic and therapeutic skills needed to treat these

patients. Depending on the goals of treatment,

special facilities or a well-equipped exercise area may

be needed for carrying out the diagnostic and

therapeutic processes diagnosis and therapy involved

in treating these patients.

Definition of COPD

COPD includes the disorders of chronic bronchitis and

emphysema. Chronic bronchitis is defined as the

presence of continuous bronchial obstruction and of

a chronic productive cough that lasts for at least three

months in each of two successive years. In making

this diagnosis, other causes of chronic coughs should

be excluded. Emphysema is present when there is

increased lung volume accompanied by destruction

of alveolar walls, without fibrosis.

Chronic bronchial obstruction is a key factor in

patients with COPD, bringing about complaints such

as dyspnea, whether during exercise or at rest or both,

and coughing, sputum expectoration, and wheezing.

The patient’s general level of fitness deteriorates

because of the disorder and its direct and indirect

consequences, such as hypoxemia, medication use,

immobility and malnutrition. Patients may tend to

avoid exercise and this causes their general

physiological condition to deteriorate further.

Consequently, there may be problems performing

normal daily life activities and psychological

complaints may develop, which can be expressed in

the form of anxiety, depression and lowered self-

esteem. In addition, the patient may become socially

isolated.

The primary causes of COPD are cigarette smoke and

occupational exposure to high-risk substances. In

Clinical practice guidelines for physical therapy in

patients with chronic obstructive pulmonary disease

GE BekkeringI, HJM HendriksII, RVM Chadwick-StraverIII, R GosselinkIV, M JongmansV, WJ PatersonVI, CP van

der SchansVII, MCE Verhoef-de WijkVIII, M DecramerIX.

I Trudy Bekkering, physical therapist and movement scientist, Research and Development Department, Dutch Institute of Allied Health

Professions, Amersfoort, the Netherlands.

II Erik Hendriks, physical therapist and movement scientist, Research and Development Department, Dutch Institute of Allied Health

Professions, Amersfoort, the Netherlands.

III Renata Chadwick-Straver, physical therapist, Department of Physical Therapy, VU Hospital, Amsterdam, the Netherlands.

IV Rik Gosselink, physical therapist, Department of Physical Therapy and Rehabilitation, Gasthuisberg University Hospital, Leuven, Belgium.

V Machteld Jongmans, physical therapist, Department of Physical therapy, Dekkerswald University Pulmonary Center, Groesbeek,

The Netherlands.

VI Bill Paterson, physical therapist, Department of Physical therapy, Dijkzigt Academic Hospital, Rotterdam, the Netherlands.

VII Cees van der Schans, physical ttherapist, Department of Physical therapy, Academic Hospital, Groningen, the Netherlands.

VIII Mirjam Verhoef-de Wijk, physical therapist and Cesar therapist, Academic Institute for Physical Therapy, Utrecht, the Netherlands.

IX Marc Decramer, pulmonary physician, Department of Pulmonary Diseases, Gasthuisberg University Hospital, Leuven, Belgium.

addition, air pollution, genetic factors and respiratory

infections can contribute to the development of

symptoms. A poorer prognosis is associated with

persistent smoking, increased non-specific hyper

responsiveness, mucus hypersecretion, hypoxemia

and weight loss. The exercise capacity of the patient,

has a positive impact on survival.

Epidemiology

In the 1960s and 1970s, a number of cohort studies

on the prevalence of asthma or COPD were carried out

in adults aged up to 65 years in the Netherlands.

They did not differentiate between asthma and COPD.

The prevalence of COPD in the Dutch population

ranges from 13.0–16.8% in men and from 4.5–7.3%

in women. On average, 2.2 new COPD patients per

1,000 adults report to primary care physicians each

year (i.e., the incidence of COPD), while 20.4 patients

out of every 1,000 adults are diagnosed with COPD

(i.e., the prevalence of COPD). Both the incidence and

prevalence rise with age and both are higher in men

than in women. Both are related to the smoking

habit.

Position of physical therapy

In the Netherlands, patients are referred to physical

therapists by either a primary care physician or a

medical specialist. The Dutch College of General

PractitionersNederlands Huisartsen Genootschap

(NHG, Dutch College of General Practitioners) has

published guidelines on the diagnosis and treatment

of adult patients with COPD. With regard to physical

therapy, these guidelines only refer to the use of

specialized facilities. A better understanding of how

physical therapy can be used in this group of patients

– for instance, by improving communication between

physical therapist and referring physician – is

important for increasing the efficiency of care in

these individuals.

DiagnosisReferral

Patients with COPD may be referred for physical

therapy after their medication has been optimized.

Furthermore, the COPD patients must haveresult in

impaired mucus clearance, disability in performing

normal daily activities due to dyspnea, impaired

exercise capacity, or a combination of these factors.

See Table 1.

COPD is accompanied by a range of impairments,

disabilities and problems with participation. The

patient’s forced expiratory volume in one second

(FEV1), a measure of airflow obstruction, is, by itself,

not a good predictor of the degree of difficulty the

patient experiences. Optimally, the referral

documentation should contain data on the severity

and nature of the airflow obstruction, the natural

course of the disorder, and relevant medical and

psychosocial factors. If exercise training is indicated,

data from an incremental exercise test at maximum

load should be included in the referral data, if the test

was carried out. These requirements imply a need for

consultation between pulmonary specialists, physical

therapists and, if involved, other healthcare

specialists.

History-taking

In history-taking, the aim is to gain the clearest

picture possible of the patient’s health problem. The

physical therapist must determine the patient’s

general needs, expectations, degree of motivation,

need for information, and (global and local) load and

load-bearing capacity, and how the patient is coping

with the disorder and its consequences. One

component of history-taking is the quality-of-life

inventory. Questionnaires such as the Chronic

Respiratory Disease Questionnaire (CRDQ) or the St

George’s Respiratory Questionnaire (SGRQ) can be used

for this purpose. Table 2 details the main points of

history-taking. More information is given below in

the review of the evidence.

2


V-03/2003/US

Physical therapy is indicated when, because of COPD, patients:

• have problems coughing up sputum and have recurrent respiratory infections; or

• have breathlessness (dyspnea) and are, therefore, limited in their daily activities, or both.

Table 1. Main reasons for referral.

On the basis of history-taking, generally two

problems can be distinguished in these patients:

impaired mucus clearance and impaired exercise

capacity including dyspnea. In practice, these two

problems often occur in combination. Patients may

also have additional problems, such as cor pulmonale

or hypoxemia, that could influence the type of

physical therapy intervention or program selected.

Physical examination

The physical examination is defined as an

examination that covers functional impairment and

disabilities in normal daily activities. The strategy

adopted in the physical examination depends on the

health problems found. Tables 3 and 4 describe the

main points of the physical examination of patients

with impaired mucus clearance and patients with

impaired exercise capacity (including dyspnea),

respectively. They also describe how data are

obtained. More information on the physical

examination and the measuring instruments used is

given below in the review of the evidence.

Analysis

The results of history-taking and the physical

examination, supplemented by medical referral data,

provide clear evidence for deciding whether to refer a

patient for physical therapy. On the assumption that

the referring physician has correctly diagnosed COPD,

the following questions should be answered:

• Are any COPD-related health problems present?

• Which functional impairments and disabilities are

observable and what problems with participation

does the patient experience?

• Which complaints, impairments and disabilities

can be affected by physical therapy?

• Is the patient motivated to undergo physical

therapy?

On the basis of the obtained data, the physical

therapist should be able to determine whether a

referral for physical therapy is justified. If there is any

3


V-03/2003/US

• Record the patient’s symptoms and current condition;

• Determine whether there are any sensations of dyspnea and, if so, whether they are experienced at rest

or during exercise;

• Determine whether there are any signs of impaired mucus clearance;

• Determine whether there are any signs of impaired exercise capacity; determine which disabilities in

normal daily activities the patient experiences because of the disorder;

• Assess quality-of-life;

• Note the natural course followed by the symptoms and the disorder;

• Note load and load-bearing capability; determine which causal or inhibitory factors are influencing

symptoms and their progression;

• Determine the patient’s need for information.

Table 2. Main points of history-taking.

Information on: Procedure Evaluation method

• signs of (severe) obstruction observation contraction of scalene muscles,

tracheal tug, Hoover’s sign

• the quantity, consistency and observation

appearance of sputum

• location of sputum observation and auscultation

• whether coughing or blowing observation and listening

is productive

• signs that airways collapse has occurred observation and listening

Table 3. Main points of the physical examination of patients with impaired mucus clearance.

doubt about the severity or nature of the disorder or

about any related health problems, the referring

physician should be consulted. The patient may need

to be referred back for additional diagnosis or to

adjust the treatment approach.

After it has been concluded that physical therapy is

indicated, it must be determined whether the

individual patient can be treated according to the

guidelines. Patients can be treated according to these

guidelines if:

• the referral data is adequate; and

• the patient’s medication has been optimized, as

discussed in the NHG guidelines on COPD.

Treatment plan

After the above questions have been answered,

individual treatment goals are drawn upformulated in

consultation with the patient, and a treatment plan is

formulated. In rehabilitation, the general goal of

treatment is to reduce or eliminate the patient’s

impairments, disabilities and problems with

participation, thereby improving quality of life.

Furthermore, for patients with COPD, the most

common treatment goals are:

1. to improve mucus clearance;

2. to improve exercise capacity;

3. to reduce dyspnea; and

4. to promote compliance with therapy.

In addition to those mentioned above, the patient

may experience other health problems, which in

some cases may be associated with the underlying

pulmonary disease. The therapist may deem these

problems to be such that further physical therapy is

indicated. However, these additional health problems

are not covered by these guidelines.

TherapyThe therapeutic process is geared to the treatment

plan, which, among other things, expresses the most

common treatment goals in patients with COPD.

4


V-03/2003/US

Information on: Procedure Evaluation method

• signs of (severe) obstruction observation contraction of scalene muscles,

tracheal tug, Hoover’s sign

• strength and endurance of skeletal measurement handheld dynamometer

muscle

• strength and endurance of measurement mouth pressure meter

respiratory muscles

• general endurance measurement 12-minute walking test, shuttle test,

cycle ergometer endurance test

• dyspnea measurement Borg scale, visual analogue scales

Table 4. Main points of the physical examination of patients with impaired exercise capacity.

• If airways collapse develops, the compressive force is too great. The risk of collapse can be prevented to

the greatest possible extent if the patient coughs or huffs with little force and starts with a large lung

volume.

• Coughing and huffing require adequate abdominal muscle strength. If there are indications that strength

is insufficient, external pressure can be applied, such as manual pressure exerted by the physical therapist

or the patient himself or herself.

• The stimulus of coughing can cause a tickling cough and bronchospasm in susceptible patients. This can

be counteracted by using as little force as possible. Pursed-lips breathing can also be used. If these

remedies are insufficient, medication use should be re-evaluated.

Table 5. Main points of treatment for improving mucus clearance.

Improving mucus clearance

In order to improve mucus clearance patients are

taught techniques that enable them to clear mucus

effectively by themselves. Long-term goals are, for

example, to ensure that fewer exacerbations of the

condition occur and to engender a less rapid

deterioration in pulmonary function, as indicated by

the FEV1 value.

For mucus clearance, coughing and blowing are

extremely important. The physical therapist should

first, therefore, choose to teach techniques for

effective coughing and blowing. By adjusting the

force used and matching it with the patient’s lung

volume, these techniques can be adjusted for the

individual patient.

If coughing or huffing does not result in the

expectoration of mucus, it may be possible to

promote mucus transport using forced expiration

techniques in combination with postural drainage.

Although the sole use of either postural drainage,

chest percussion or vibration, or positive expiratory

pressure has not been unequivocally substantiated by

the literature, when used in various combinations

these techniques may be effective in individual

patients. If these procedures prove not effective after

six sessions, their continued use is no longer

meaningful. Exercise can help some patients clear

mucus secretions. To encourage mucus clearance,

however, the patient must ventilate substantially .

Then, the normal conditions for exercise training

apply.

Effective procedures for mucus clearance should lead

to the expectoration of mucus, or to a reduction in

rhonchi, either during treatment or within 30

minutes after treatment. The treatment goal will have

been achieved when the patient is able clear mucus

by himself or herself.

Improving exercise capacity

The review of the evidence below describes five

reasons for reduced exercise capacity in these

patients. The different reasons for reduced exercise

tolerance can be distinguished using an incremental

exercise test at maximum load that also involves the

measurement of blood gas concentrations. In

practice, reduced exercise capacity is usually caused

by several factors. For didactic purposes, these factors

will be discussed separately here. By using the

information presented below, the physical therapist

can concentrate on certain aspects of treatment

depending on the individual patient’s needs.

Exercise capacity can be improved in two main ways:

firstly, by increasing efficiency of movement and,

secondly, by achieving a physiological training effect.

Training aimed at improving exercise capacity should

last a minimum of six weeks and a maximum of six

months. Training should be given at least three times

per week for 20–45 minutes. A physiological training

effect occurs when the body has to work against

increasing load. To achieve this, a minimum level of

intensity must be used (see the discussion on

cardiocirculatory limitations below).

1. Cardiocirculatory limitations

In training1 to increase overall exercise capacity, the

general principles for improving physical condition

5


V-03/2003/US

• A good breathing technique is necessary for training to build exercise capacity. The breathing technique

should be adjusted for the individual patient.

• In each exercise program, attention should be paid to all the functions that are important for physical

performance, such as muscle strength, muscle endurance, speed, coordination and flexibility. Different

forms of exercise can be used, such as circuit training, sports and games, or swimming.

• Moderation is important in COPD patients. Depending on the Borg scale score or heart rate, for instance,

one patient may need to be encouraged to become more active whereas another may need to be held

back.

Table 6. Main points of treatment for improving exercise capacity.

1. The (Dutch) Classification of Procedures for Paramedical Professions (CVPB) uses the terms exercising and guidding.

6


V-03/2003/US

can be applied. To improve exercise capacity (i.e., to

obtain a physiological training effect), one must

exercise at least three times a week for 20–45 minutes

at 60–80% of maximum heart rate. Sessions may

consist of one or more forms of exercise, such as

cycling, walking, climbing stairs and rowing. The

training effect is specific: in other words,

improvement will occur primarily in the activity

being trained. This means that the program content

must be geared to the desired activity, to the patient’s

needs, and to the patient’s main health problems. To

retain effects of the treatment after the conclusion of

therapy, exercise frequency is reduced to once or

twice a week at the same intensity.

2. Ventilatory limitations

In addition to providing a general exercise program,

inspiratory muscle training (IMT) can also be given.

These two elements are discussed separately.

General exercise program

Patients whose exercise capacity is limited by

ventilation problems can receive endurance training

unless hypoxemia (i.e., an oxygen saturation < 90%)

or severe hypercapnia (i.e., an arterial carbon dioxide

pressure > 55 mmHg) is present during exercise.

Training load is determined by the results of the

incremental exercise test, with training aiming for

60–80% of maximum load for an exercise duration of

at least 20 minutes. If hypoxemia or severe

hypercapnia is present, exercises should be carried

out using intervals . Most commonly, sequences of

two minutes of exercise followed by two minutes of

rest are repeated for a total of, at least, 20 minutes.

Even for patients who experience increased

obstruction when exercising (e.g., patients with

unstable airways), interval training is the correct way

of increasing exercise capacity. Some practical

examples are circuit training and interval walking or

cycling protocols.

Inspiratory muscle training

A prerequisite for giving inspiratory muscle training

is that the patient has diminished inspiratory muscle

strength or endurance. To determine whether this is

the case, the physical therapist should measure the

maximum inspiratory pressure at the mouth (PImax).

Reference values are given in Note 12 of the notes on

diagnosis at the end of the review of the evidence.

The appropriate equipment and expertise are required

to perform these measurements correctly. The value

of PImax determines the selection of the exercise

load. In order to train the inspiratory muscles, there

must be some inspiratory resistance. Resistance can

be either flow-dependent or flow-independent (i.e.,

threshold).

To increase the strength and endurance of the

respiratory muscles, the patient should exercise twice

daily for 15 minutes at a load level of at least 30–40%

of PImax. PImax must be measured regularly, so that

exercise intensity can be adjusted during the exercise

program, if necessary. After completion of the

exercise program, respiratory muscle strength must be

• If the form of exercise chosen is different from that used in the incremental exercise test, the baseline

exercise level should produce the heart rate reached at 60% of maximum load during the test. One

should also take the Borg scale score into account in setting the exercise load.

• In this patient group, hypoxemia can develop during exercise. The incremental exercise test at maximum

load could verify this. Since hypoxemia can lead to cardiac arrhythmia, the physical therapist must

measure oxygen saturation either regularly or continuously in these patients.

Table 7. Main points of exercise programs for patients with ventilatory limitations.

• When flow-dependent inspiratory resistance is used, the patient should be given feedback on the

pressure and flow rate used to reach the target levels (i.e., target flow rate or target pressure) during

training. An in-line pressure gauge or flowmeter can be used for this purpose.

Table 8. Main points of respiratory muscle training in patients with a ventilatory limitations.

maintained. This can be achieved by exercising at the

same intensity 2–3 times a week for two 15-minute

sessions .

3. Oxygen transport limitations

Oxygen transport limitations can result in a

desaturation during exercise. Therefore, the physical

therapist must measure oxygen saturation regularly

or continuously during training. Imminent

hypoxemia can be prevented by supplemental

oxygen therapy. The administration of oxygen is

classified in the same way as providing medication

and can only be prescribed by a pulmonary

physician, who is then responsible for treatment.

Therefore, treatment involving the administration of

oxygen should be carried out in specialized facilities.

If patients are willing, their training can take place in

a primary care facility, provided the physical therapist

has an oxymeter to monitor saturation during

treatment.

When training to increase exercise capacity in these

patients, interval training should be used unless

oxygen supplementation is prescribed. Exercise

intensity depends on the results of the incremental

exercise test. The patient should start with an exercise

load at which oxygen saturation is more than 90%,

unless otherwise indicated by the pulmonary

physician. If supplemental oxygen is given, the target

exercise load can be 60–80% of maximum load. In

addition to training exercise capacity, the physical

therapist may also teach the patient how to use his or

her physical capabilities as efficiently as possible.

Since this is more a matter of ergonomics, it would be

helpful if an occupational therapist specializing in

COPD is consulted or cooperates in treatment.

For these patients, the application of ergonomics

involves exercises aimed at improving the

performance of normal daily activities. In addition,

patients can also practice breathing exercises, such as

breathing at a slow rate with pursed lips. This may

help achieve more effective ventilation and, thereby,

a higher oxygen saturation at rest.

4. Peripheral muscle weakness

For patients with peripheral muscle weakness, an

endurance training program should be given (see the

description under cardiocirculatory limitations above)

unless hypoxemia (i.e., an oxygen saturation < 90%)

or severe hypercapnia (i.e., an arterial carbon dioxide

pressure > 55 mmHg) develops, in which case interval

training is indicated. Other functions , such as muscle

function, velocity, coordination and flexibility, also

need to be trained. Exercise load should be at least

60% of maximum load. The target exercise load

should be as high as possible for the desired duration.

In the training program, additional attention needs

to be given to improving the functioning of relevant

muscle groups.

In giving exercises to strengthen arm and leg muscles

and to improve their endurance, general training

principles apply. The patient should train three times

a week. A training regimen that emphasizes both

strength and endurance is usually employed. An

exercise load of about 60% of maximum and exercises

involving 10–30 repetitions are appropriate.

7


V-03/2003/US

Table 9. Main points of treatment for patients with oxygen transport limitations.

• If the transfer coefficient (TLco), which indicates the diffusion capacity of the lungs, is less than 50%

predicted, the risk of hypoxia occurring during exercise is very high. In these patients, it is essential to

pay extra attention to measuring oxygen saturation during exercise.

• Good nutrition is important if muscle strength is to be increased. Hypoxemia, inactivity, and, especially,

the use of oral corticosteroids all have a negative impact on muscle function. If any of these factors is

contributing to peripheral muscle weakness, it should be eliminated or its effects should be reduced.

Consultation with the relevant specialist is desirable.

Table 10. Main points of treatment for patients with peripheral muscle weakness.

5. Other factors

One other factor that influences exercise capacity is

an inadequate breathing pattern due to exercise

phobia. The patient might not have been able to

achieve his or her maximum performance during the

cycle ergometer test because of fear of bronchospasm,

dyspnea or stress. In addition, other disorders or

diseases may also have this effect.

Patients in this group can be offered an endurance

training program (see the description under

cardiocirculatory limitations above) unless

hypoxemia (i.e., an oxygen saturation < 90%) or

severe hypercapnia (i.e., an arterial carbon dioxide

pressure > 55 mmHg) develops, in which case

periodic training is indicated. Other functions, such

as muscle function, velocity, coordination and

flexibility, also need to be trained. This patient group

should begin with a very low exercise load. However,

the exercise load should be at least 60% of maximum

load and the target exercise load should be as high as

possible for the desired duration. If anxiety or stress is

contributing to the reduced exercise capacity,

relaxation exercises can be given.

Reducing dyspnea

Dyspnea has multiple causes. In treatment, therefore,

it is important to employ a range of different

approaches and to determine which is most effective

for the individual patient.

Optimizing diaphragm function

The slight contraction of the abdominal muscles

during expiration can facilitate diaphragm function.

This action positions the diaphragm optimally for the

next inspiration, resulting in a better function. In

addition, the patient can assume certain body

postures that lengthen the diaphragm, enabling it to

contract more efficiently. One example is leaning

over from a sitting position. The accessory muscles of

respiration can provide more force if the arms are

anchored in position, for example, if the patient

walks with the aid of a rollator walker or uses

handrails.

Increasing tidal volume and lowering breathing

frequency (at rest)

There are a range of different breathing exercises for

increasing the ratio of inspiration time to expiration

time. The key is to shorten inspiration relatively and

prolong expiration. This process helps patients

become aware of their breathing and gives them the

sense that they can control it and that they can even

contribute to managing their symptoms. Increasing

tidal volume and reducing the breathing rate improve

alveolar ventilation.

During pursed-lips breathing, the patient exhales

gently against slightly pursed lips. This causes the

tidal volume to increase and the frequency of

breathing to decrease. Some patients may already do

this spontaneously.

Increasing the strength and endurance of

respiratory muscles

Inspiratory muscle training can reduce dyspnea

because it increases the load-bearing capacity of the

respiratory muscles. See the discussion of ventilatory

limitations above.

Optimizing ergonomic factors

During treatment, it is important to pay attention to

ergonomic factors. This can involve giving the advice

to alternate periods of efforts with rest. The presence

of a severe obstruction can be a reason for deciding to

assess whether a patient might benefit from different

kinds of mobility aids. This could be done in

consultation with a specialized occupational

therapist, for instance. Examples of such aids are

walking aids (e.g. a rollator walker) or home

8


V-03/2003/US

Table 11. Main points of treatment for patients with dyspnea.

• In patients with COPD, the breathing pattern is usually functional. Therefore, the physical therapist

must always ensure that any change in breathing movement is an improvement for the individual

patient.

• Not all patients find pursed-lips breathing pleasant.

9


V-03/2003/US

adjustments (e.g. the installation of a stairlift).

Desensitization

Repeated experiencing of dyspnea, for example,

during exercise in a safe environment, can reduce the

perception of dyspnea.

Improving compliance with therapy

A significant goal in ensuring therapeutic compliance

is bringing about behavioral modification. For

treatment to have lasting results, patients have to

incorporate the functions and skills learned during

treatment into their daily lives. For COPD patients, this

almost always involves complying with therapy over

the long term.

The physical therapist has a role in training the

patient in and educating the patient about the

behavioral adjustments and modifications required.

Patient education should be considered as a means of

achieving behavioral modification. Consequently,

patient education is a significant aspect of care.

A professional approach to patient education

presumes knowledge about and understanding of

how information can be presented and of the factors

that positively or negatively influence the

development of the desired behavioral modification.

Before beginning patient education, the patient’s

need for information about and training in the new

behavior must be assessed. These needs provide the

starting point for the education program. Patient

education can be subdivided into four categories:

information, instruction, education and guidance. In

practice, these four categories overlap one another. In

each category, activities require different amounts of

time, and make different demands on equipment and

on the therapist’s skills.

To achieve behavioral change, the patient must pass

through six stages:

1. being open to information about the need to

change behavior;

2. understanding and remembering the information;

3. wanting to change behavior;

4. being able to perform the modified behavior;

5. actually performing (doing) the behavior; and

6. continuing to perform the behavior over the long

term.

Analyzing the process in term of these different stages

helps in achieving an understanding of the problems

involved in therapeutic compliance. It is essential for

behavioral modification that patients have

confidence in their own capabilities (i.e., their self-

efficacy) and that the advantages of behavioral

modification outweigh the disadvantages. More

information is given in the review of the evidence.

Completion and reportingAt some point during treatment and, mandatory, at

the end of treatment, the referring physician should

be informed about the goals of treatment, the

treatment carried out and the results of treatment in

the individual patient. Communication will also have

to take place about the division of responsibilities

during rehabilitation and about any necessary

consultation with other health professionals.

After-careAfter treatment has ended, follow-up in the form of

providing after-care will be necessary. After-care is

Table 12. Main points of patient education.

• Patient education must be presented in a structured form. In other words, not too much information

should be given at once and the information should be sequenced in a way that makes sense to the

patient.

• Information given to the patient must be customized. In other words, the patient’s characteristics and

social environment must be taken into account.

• The physical therapist must continuously monitor whether the patient experiences any problems in

practicing exercises or in implementing behavioral modifications, and must provide help in working

through these issues.

provided on the condition that there are no medical

grounds for further treatment. The goal of after-care

is to ensure that the benefits of therapy are

maintained. Patients who receive after-care in a group

can derive additional benefits from contact with

peers.

In the Netherlands, the Dutch Asthma Foundation

(Nederlands Asthma Fonds) organizes athletic groups

for individuals with COPD. These involve participation

in specially adapted group sports and games. Peer

contact plays an important role in maintaining the

newly learned behavior. COPD athletic groups are

coached by physical therapists who specialize in

COPD. No suitable course of action has yet been found

for the category of patients who are not eligible to

attend COPD athletic groups (see the exclusion criteria

noted in the discussion on after-care in the review of

the evidence section).

10


V-03/2003/US

Table 13. Main points of after-care.

• Over the long term, patients find it easier to continue practicing forms of movement they enjoy. It also

appears easier to continue practicing in a group.

• Scheduling check-ups during after-care increases the patient’s motivation to maintain the behavioral

change and the state of health achieved.

11


V-03/2003/US

Introduction

The KNGF-Guidelines COPD deals with the physical

therapy treatment of patients with Chronic

Obstructive Pulmonary Disease (COPD), namely

chronic bronchitis and emphysema. The guideline

includes the diagnostic and therapeutic process in

line with the methodical therapeutic conduct.

Definition

KNGF-guidelines are defined as ‘guidelines whose

production is directed by a central body, that are

developed systematically, that are written by

experts, and dhat deal with the systematic process

of physical therapy in certain health problems

and with various (organizational) aspects of the

profession’.1,2

Objective of the KNGF-guidelines COPD

The objective of the guidelines is to describe the

‘optimal’ diagnosis and physical therapy treatment –

with regard to effectiveness, efficiency and tailored

care - for patients who have, due to COPD,

impairments in the mucus clearance or who

experience disabilities in ADL due to dyspnea or who

have exercise limitations. The recommendations are

based upon current scientific research, professional

and social insights.1-3

Besides the above mentioned goals, the KNGF-

guidelines are explicitly meant to:

• Change the care in the desired direction based on

current scientific research and improve the quality

and the uniformity of this care.

• Assure insight into tasks and responsibilities and

to stimulate cooperation.

• Support the process of decision making with

regard to the treatment or not and the use of

diagnostic and therapeutic interventions.

To make use of the guidelines it is necessary to insure

the recommendations of professional requirements.

Presenting the clinical questions

The group which has formulated these guidelines

wanted to attain an answer on the following

questions:

• Which factors can be influenced by physical

therapy?

• What is the objective of physical therapy?

• Which parts of the physiotherapeutic diagnostic

assessment are valid, reliable and useful in daily

practice?

• Which forms of treatment and prevention are

clinical significant?

Formation of the mono disciplinary working

group

In July 1996 a mono disciplinary working group of

professionals was formed to answer these clinical

questions.3 In the formation of the working group an

attempt was made to achieve a balance in

professionals with experience in the area of concern

or with an academic background. All members of the

working group have stated that they had no

conflicting interests what so ever in relation to the

development of the KNGF-guidelines. The

development of the guidelines took place from July

1996 until December 1997.

Procedure of the mono disciplinary working group

The guidelines have been developed according to the

‘Methods for the Development and Implementation

of Clinical Guidelines’.1-5 This method includes

practical instruction of the strategies used to collect

literature. In the continuation of the review of

evidence in these guidelines the specific terms used

for the search, the sources used, the period in which

the literature was published, and the inclusion or

exclusion criteria for the literature are mentioned.

For a more extensive description of the different

literature searches is referred to the background

report : The physical therapeutic interventions in

patients with chronic obstructive pulmonary

diseases.3

The members of the working group have individually

selected and graded the proceedings attaining to the

scientific evidence. Even though the scientific

evidence is prepared by individuals or by smaller

subgroups, the result is laid out and discussed within

the whole working group. The scientific evidence is

then summarized in a conclusion, including the

Review of the evidence

12


V-03/2003/US

extent of the evidence. Besides the scientific evidence

there are other important aspects for making the

recommendations such as: reaching a general

consensus, efficiency (costs), resource availability,

necessary expertise and education, organization

aspects and the attempt for agreement with other

mono or multi disciplinary guidelines.1-3 If there was

no scientific evidence available, the

recommendations were formulated based upon

consensus within the working group or secondary

group of professionals.

The recommendations are commented on by external

professionals. Once the mono disciplinary concept

guidelines were completed they were sent to external

professionals and/or occupational organizations

(secondary working group) to attain a general

consensus within the other occupational groups or

organizations and/or with other mono and multi

disciplinary guidelines. Also the wishes and

preferences of patients are taken into account by

representation of the Dutch Asthma Foundation.

Validation by the intended users

Before publication and distribution, the guidelines

are reviewed and systematically tested by the

intended users (validation). The concept of the KNGF-

guidelines COPD was sent to a group of 64 physical

therapists working in different working environments

to judge the guidelines. The comments and remarks

from the physical therapists are documented and

discussed in the working group and if possible or

desired included in the final guidelines.

The recommendations for the practice are the result

of the available evidence, the above mentioned other

aspects and the results of testing the guideline

amongst the intended users.

Constitution, products and implementation of the

guidelines

The guidelines exist of three parts: the practical

guideline, a schematic layout of the main points of

the guideline (summary) and the review of evidence

section. All parts of the KNGF-guidelines can be read

separately. After the publication and distribution of

the guidelines amongst members of the KNGF, an

article on the most important recommendations has

been published6 and a segment promoting

professionalism has been developed and published to

stimulate the use of the guidelines in daily practice.7

The guidelines are implemented according to a

standard of implementation strategies which are

described in the method.1-5,8

Nomenclature

Orie et al.9 firstly introduced the term chronic non-

specific lung disease (CNSLD) in the 1960s. Sluiter et

al.10 continued to use this umbrella term because

they believe there is a substantial overlap between the

disorders of asthma, chronic bronchitis and

emphysema, and furthermore that these conditions

have the same pathogenesis and pathophysiology.

They hold that the distinction made between these

disorders is neither very plausible nor meaningful. In

addition to using the term CNSLD, criteria that better

delineate the patient group must also be defined.10

Outside the Netherlands, however, the term CNSLD is

rarely used.11 Moreover, in recent years, there have

been increasing indications that there is a great

difference between the disorders of asthma and COPD.

Any confirmed distinction between asthma and COPD

would have a significant impact on therapy and

prognosis.12,13

Introduction to these guidelinesTarget group

Specific and demonstrable knowledge and skills are

required for adequately treating patients with COPD.

The necessary knowledge and skills can be obtained

by having extensive experience working with these

patients or through continuing education, which

should include learning about pathology, the

mechanics of breathing, general training principles,

measuring instruments, and the interpretation of

incremental exercise test results. The special

requirements placed on the treatment environment

and equipment used should also be covered. The

treatment area must be clean and well-ventilated.

There must also be an area where patients can rest for

short periods, change their clothing and wash. A

mouth pressure meter is required for testing and

training inspiratory muscle strength. Equipment for

exercise training includes a treadmill or cycle

ergometer, exercise apparatus, an exercise mat, and a

pulse oximeter.14 When treating patients with

impaired oxygen transport, equipment for oxygen

supplementation must be available. This equipment

could belong to the patients themselves.

Defining COPD

The American Thoracic Society uses the following

definitions.15 Chronic obstructive pulmonary disease

(COPD) is characterized by airflow obstruction due to

chronic bronchitis or emphysema. The, partially

reversible, obstruction tends to be progressive and

may be associated with airway hyper reactivity.

Chronic bronchitis is defined as the presence of a

chronic productive cough that lasts for at least three

months in each of two successive years. In making

this diagnosis, other causes of chronic coughs should

be excluded. Emphysema is present when there is

abnormal permanent enlargement of the lung

accompanied by destruction of alveolar walls,

without fibrosis.15

Pulmonary function tests can be useful in making a

diagnosis and in indicating the severity of the

disorder. The European Respiratory Society states that

measuring the forced expiratory volume in one

second (FEV1). provides an indication of the severity

of the disorder.16 The American Thoracic Society has

used FEV1 to indicate the different stages of COPD,17 as

shown in Table 14.

Although FEV1 is used to indicate the severity of

pulmonary disease, this measure has not been found

to be a good predictor of quality of life nor of the

disabilities experienced by patients. Various trials

have shown that there is only a weak relationship

between pulmonary function and health-related

quality of life in COPD patients.18–21 Williams et al.22

found a weak correlation between pulmonary

function and disabilities, and a strong correlation

between dyspnea and disabilities. Okubadejo et al.20

studied the correlation between FEV1 and the results

of using the St George’s Respiratory Questionnaire

(SGRO), the Sickness Impact Profile, and the Hospital

Anxiety and Depression Scale. Only the relationship

between activity on the SGRO and FEV1 was found to be

significant. In general, levels of anxiety and

depression were found to be better predictors of

quality of life than physiological parameters.

COPD mainly affects people in middle age. Common

symptoms are dyspnea with coughing, wheezing,

sputum production, and recurrent respiratory

infection.23 Compared to persons in a normal cross-

section of the population, COPD patients have more

disabilities in their daily live. A Dutch study of 50

COPD patients found that 46% were unable or only

partly able to hold a job or keep house because of

their condition. In addition, patients were

handicapped in carrying out physical activities

involving exertion.24 Problems with mobility, vitality

and sleep, and emotional problems such as

depression and anxiety were also experienced. Social

problems took the form of difficulties in performing

housework and leisure activities, and reduced social

interaction.19

Causes

The prevalence of coughing and sputum production

is higher in smokers,25 who also exhibit a greater

annual decline in FEV1.26–28 In addition, the mortality

rate due to copd is higher in smokers.29 Increased

smoking accelerates the decline in FEV1, whereas

ceasing smoking slows the decline in FEV1.30 A study

carried out by Kauffmann et al.30 showed that

occupational exposure to certain materials was

13


V-03/2003/US

FEV1 (% of predicted value)

European Respiratory Society mild ≥ 70%

moderately severe 50–69%

severe 35–49%

American Thoracic Society phase 1 ≥ 50%

phase 2 35–49%

phase 3 < 35%

Table 14. Two classifications of COPD severity based on measurement of forced expiratory volume in one

second (FEV1).

related to decreased FEV1. Heederik at al.31 found

relationships between occupational exposure to

certain substances, such as smoke, dust and metals,

and respiratory symptoms and pulmonary function

disorders. In addition, there are several other factors

that may be associated with copd, such as air

pollution (both indoor and outdoor), passive

smoking, socioeconomic status, genetic factors,

respiratory infection, allergy, bronchial hyper

responsiveness, age and sex.32

Prognosis

In the medical literature, a connection is usually

made between prognosis and survival. The strongest

predictors of mortality are age and FEV1. The higher

the patient’s age and the lower his or her FEV1, the

worse the prognosis.33,34 After correcting for age and

FEV1, total lung capacity, heart rate at rest, and the

degree of physical limitations and disabilities

experienced all appear to correlate positively with

mortality. Exercise capacity appears to have a

negative correlation with mortality.33

Chronic mucus hyper secretion is related to a more

rapid decline in FEV1 and is a predictor of death from

respiratory infections in COPD patients.34 Weight loss

is also associated with a poorer prognosis.35

Postma et al.36 established that deterioration in FEV1 is

determined by the degree of bronchial hyper

responsiveness, the reversibility of bronchial

obstruction, and whether the patient ceases smoking.

The more severe the hyper responsiveness, the more

rapid the deterioration. The better the reversibility,

the slower the deterioration. Smoking cessation has a

positive effect on survival and on FEV1 decline over

time.

Epidemiology

The most extensive longitudinal cohort study on the

prevalention of COPD, in which no distinction was

made between asthma and COPD, was conducted

between 1965 and 1969 in the Netherlands: the

Vlagtwedde-Vlaardingen study.37 Another study, the

Zoetermeer Epidemiological Preventive Study was

carried out between 1976–1978.38 These trials found

that the prevalence of COPD in men varies from

13.0–16.8% and, in women, from 4.5–7.3%.

In the period 1985–1988, morbidity records were

maintained by Dutch primary care physicians at the

Nijmegen University Primary Practice Institute. These

showed that the incidence and prevalence of COPD is

higher in men than women and that both measures

increase with age in both sexes. In men, the

incidence increases from 0.2 per 1,000 in the 25–34

year age group to 24.4 per 1,000 in those aged 75

years and older; in women, from 0.4 per 1,000 in the

25–34 year age group to 4.2 per 1,000 in those aged

75 years and older. In men, the prevalence increases

from 6.6 per 1,000 in the 25–34 year age group to

233.9 per 1,000 in those aged 75 years and older; in

women, from 4.0 per 1,000 in the 25–34 year age

group to 43.9 per 1,000 in those 75 years and older.38

These figures probably give underestimates because

not all COPD patients are registered with their primary

care physician as having the condition.

Combining these figures from the Nijmegen

University Primary Practice Institute with the

demographic changes expected in coming years

indicates that an increase in the number of COPD

patients can be anticipated in the future, particularly

in the 45–64 year age group.38

Work absenteeism

The average duration of sick-leave in the Netherlands

is 22 days, when calculated from all cases of illness

notified to companies. The average illness durations

for patients with chronic bronchitis and emphysema

are 77 and 167 days, respectively.39

In 1985, the total number of sick-leave days due to

obstructive pulmonary disease comprised 1.18% of all

days lost because of diagnosed sickness in the

Netherlands, which was 612,100. Of those, 167,000

sick-leave days were due to chronic bronchitis and

61,100 to emphysema.39 These data only cover cases

of sick-leave known to company organizations and to

employers who, either jointly or as a group bear the

medical insurance risk on an ongoing basis.

Position of physical therapy

In the Netherlands, patients can be referred to

physical therapists by primary care physicians or

medical specialists. The Dutch College of General

Practitioners (NHG) recently revised its primary care

14


V-03/2003/US

guidelines for the diagnosis and treatment of COPD

patients. With regard to physical therapy, these

guidelines only refer to the use of specialized

facilities. However, recent trials on the outcome of

physical therapy have found that it deserves a role in

the treatment of patients with asthma and COPD.40-42

Only 1.7% of all physical therapy work carried out in

the primary care sector involves patients with

breathing problems.43 This is also consistent with

data on the referral policies of primary care

physicians: 89.0% of COPD patients are not referred to

other practitioners by primary care physicians, 9.0%

are referred to specialists, and only 1.8% are referred

to physical therapists.44 Possible reasons for the small

number of physical therapy referrals are that primary

care physicians may be relatively unfamiliar with the

forms of diagnosis and treatment that physical

therapists can provide for COPD patients, and that

primary care physicians may judge the severity of

obstructive pulmonary disease solely on the basis of

pulmonary function.45 This may occur despite the

fact that pulmonary function is a poor predictor of

quality of life and is a poor indicator of the quality of

life, perceives disabilities or exercise capacity,46 and of

the level of dyspnea. Having a physical therapy

consultation before referral is considered could

provide a way of clarifying the need for physical

therapy. The introduction of a consultative physical

therapy examination is one way of improving the

efficiency of care.47 The primary care physician’s

requirements from consultation can better be

satisfied by a physical therapist who has extensive

experience or who is well-trained, or both.47 In

addition, the present guidelines can also contribute

to increasing understanding of how physical therapy

can be used, thereby leading to more specific referrals

and to more knowledge of the possibilities of physical

therapy treatment .

In 1991, a study carried out at the secondary care

level in the Netherlands found that 3% of the total

number of COPD inpatients in a general hospital were

receiving treatment from physical therapists.48 No

data are available on the intervention the physical

therapists used with these patients in either primary

or secondary care, nor on the severity of the disorders

or the patients’ needs.

Pathophysiology

Bronchial obstruction is the core complaint in

patients with COPD. It can be caused by swelling of the

mucosa, the accumulation of mucus, loss of elasticity

of the lung parenchyma, or bronchospasm. These

phenomena can occur in various combinations.

Severity of bronchial obstruction

Bronchial obstruction can be quantified by measuring

dynamic pulmonary function parameters. In

particular, the maximum forced expiratory volume in

one second (FEV1) is useful. In its more severe form,

COPD may be associated with hyperinflation. In this

situation, the thorax is in a position characteristic of

inspiration when the patient is at rest. Hyperinflation

can result in a thoracic breathing pattern and an

increased load on respiratory muscles. Some clinical

observations related to the severity of obstruction are:

contraction of the scalene muscles, tracheal tug (i.e.,

downward movement of the trachea during

inspiration), and Hoover’s sign (i.e., inward

movement of the costal wall of the lower ribs during

inspiration). There are significant correlations

between these symptoms and FEV1.41 Inter-assessor

reliability is fair for observations of intercostal

retraction of the intercostal spaces, tracheal tug on

inspiration, and Hoover’s sign (Kappa minimum =

0.50, p < 0.0001 for all three symptoms).49

The typical problems affecting COPD patients that also

influence physical therapy are discussed sequentially

below.

Impaired mucus clearance

Mucus retention is very common in patients with

COPD. It can cause bronchial obstruction. In turn,

mucus retention can be caused by increased mucus

secretion or by impaired mucus transport.

Richardson and Peatfield.50 give an overview of

mechanisms that can increase mucus secretion . The

inhalation of dust or cigarette smoke increases mucus

secretion, and inhaling antigens that stimulate

inflammatory processes increases mucus production.

Impaired mucus transport may be the result of

reduced mucociliary clearance or reduced expiratory

airflow. Research carried out by Goodman et al.51

shows that smoking can result in inactive cilia.

15


V-03/2003/US

16


V-03/2003/US

Recurrent infection can lead to a loss of ciliated

epithelium.52 The contribution airflow makes to

mucus transport depends on expiratory airflow

velocity, which is determined by the magnitude of

the airflow and bronchial tube diameter.53 Effective

mucus transport occurs at high airflow velocities. To

achieve this, airflow must be large and the total

airway cross-section must be small.

Peripheral airway obstruction restricts airflow in the

peripheral airways. In turn, reduced airflow in the

peripheral airways slows airflow in the central

respiratory tracts. This process could diminish the

efficacy of mucus transport caused by expiratory

airflow.

Mucus retention can cause pathological changes in

the lungs54, possibly because of recurrent respiratory

infection. It can even contribute to the progression of

pulmonary disease.55 The presence of hypersecretion

is a risk factor for death from COPD. Hypersecretion

leads to a greater annual decline in FEV134 and is a risk

factor for hospitalization due to COPD.56 Physical

therapy can help patients use external effort to

improve mucus transport to the greatest extent

possible and several interventions are available for

doing this (see the discussion below on therapy for

improving mucus clearance).

Reduced exercise capacity

During exercise, muscle metabolism increases

resulting in more muscle oxygen consumption and

increased carbon dioxide production. Therefore,

during exercise, additional oxygen must be

transported and additional carbon dioxide must be

removed. Folgering and van Herwaarden57 designate

four types of problems that can cause decreased

exercise capacity:

1. cardiocirculatory limitations;

2. ventilatory limitations;

3. oxygen transport limitations; and

4. psychogenic limitations.

These different types of limitation can be

distinguished with the aid of an incremental exercise

test carried out at maximum load, during which

blood gas levels are also measured.

1. Cardiocirculatory limitations

In patients with mild forms of bronchial obstruction

(i.e., FEV1 > 60% of that predicted), reduced exercise

capacity may be caused by cardiocirculatory

limitations.58 In these individuals, the circulation

cannot transport an adequate amount of oxygen to

the muscles. Because of a lack of oxygen, muscles

switch to anaerobic metabolism, which involves the

production of lactic acid.58 Cardiocirculatory

limitations are demonstrated by the age-related

reduction in maximum heart rate (i.e., 220 beats/min

minus age in years) and by a blood lactate level of

approximately 10 mmol/l.57 Endurance training can

contribute to improving exercise capacity.

2. Ventilatory limitations

In patients with moderate to severe forms of

obstruction (i.e., FEV1 < 60% of that predicted), the

respiratory pump may be overloaded by

hyperinflation, dynamic collapse, or other factors.

The presence of ventilatory limitations is indicated by

increased arterial carbon dioxide pressure (PaCO2)

during the incremental exercise test.

Ventilatory limitations can be seen as being due to an

imbalance between the load on and the load-bearing

capacity of the respiratory muscles. Respiratory

muscle load is increased by increased airways

resistance and decreased compliance of the lungs and

chest wall. At the same time, the strength (i.e., the

load-bearing capacity) of the respiratory muscles may

be impaired by hypoxemia,59 hypercapnia,60 cardiac

decompensation,(61) oral corticosteroid use,63 or

malnutrition.62,64

By measuring maximum inspiratory pressure at the

mouth (PImax), the physical therapist can obtain a

reliable indication of the strength of the inspiratory

muscles.65 The clinical signs of fatigued, or heavily

loaded, respiratory muscles are an elevated respiratory

rate and, at a later stage, abdominal paradox and

respiratory alternans.66 (Abdominal paradox is

inward movement of the abdominal wall during

inspiration and respiratory alternans is alternation

between a thoracic and abdominal breathing

pattern.) Respiratory muscle fatigue can cause

respiratory failure, resulting in the development of

hypoxemia and hypercapnia. In patients with

ventilatory limitations, the maximum voluntary

ventilation threshold can be surpassed at a certain

exercise level. However, ventilation can be increased

by increasing the tidal volume and by a relative

lengthening of the expiration time. To achieve this,

the respiratory muscles, including accessory

respiratory muscles, must work harder.

Ventilatory capacity can be increased by targeted

training of the respiratory muscles. Respiratory

muscle function can be improved by increasing the

strength or endurance, or both, of the respiratory

muscles.

3. Oxygen transport limitations

In patients with oxygen transport limitations, the

alveolar capillary membrane surface area is reduced.

This causes problems with oxygen diffusion and

contact time.67 In these patients, arterial oxygen

tension (PaO2) drops during submaximal exercise.

This can only be detected using an incremental

exercise test at the patient’s maximum exercise rate.

This group of patients must learn to use their bodies

more efficiently. Breathing exercises aimed at

lowering the respiratory rate can reduce the dead

space. Furthermore, supplemental oxygen may be

necessary to improve the patient’s exercise capacity

(68–70). Training with oxygen supplementation

improves the condition of the peripheral muscles

because the number of capillaries increases and there

are more and larger mitochondria, thereby enabling

better oxygen extraction to take place. Therefore,

better use is made of the limited amount of oxygen

present.57

4. Psychogenic limitations

If a patient stops the exercise test without having

encountered one the above limitations, it can be

assumed that the reasons for stopping are

psychogenic, for example, anxiety or exercise phobia.

In all patients with psychogenic limitations, physical

therapy can help reduce the symptoms that limit

exercise. In the clinical guidelines above, these

limitations are dealt with under the category of other

factors.

Recently, a fifth type of problem that can result in

reduced exercise capacity has been described, namely:

5. Peripheral muscle weakness

If the leg muscles become rapidly fatigued, the COPD

patient’s exercise capacity will be limited.71 Recent

research by Maltais et al.72 confirms this view. The

researchers showed that patients with COPD have

reduced aerobic capacity, with the result that lactic

acid is produced at an earlier stage during exercise.

Gosselink et al.73 concluded that pulmonary function

and peripheral muscle strength are important

determinants of exercise capacity in COPD patients.

Possible causes of general muscle weakness are cardiac

decompensation,74 corticosteroid use,63 and an

impaired nutritional stage.62,64,75

Patients with peripheral muscle weakness commonly

score very high on the Borg scale for ‘heaviness’ (i.e.,

leg fatigue). during maximum exercise. In order to

confirm that muscle weakness is the reason for

stopping exercise, additional examinations should be

performed, such as testing quadriceps muscle

strength. If the peripheral muscular strength is, at

least partly, responsible for reduced exercise capacity,

then peripheral muscle training will have to be part

of physical therapy. If hypoxemia, steroid therapy or

malnutrition contribute to reduced muscle strength,

these factors should be minimized or eliminated as

far as possible. In this regard, it should be noted that

consultation with the practitioners of other

disciplines is essential for optimal treatment.

Dyspnea

Dyspnea is the unpleasant subjective sensation of

needing to breathe, which may be due to various

mechanisms:

• Central respiratory center activity is closely

associated with sensations of dyspnea.76 The

respiratory center can be activated by changes in

blood gas concentrations, such as an increase in

arterial carbon dioxide tension (hypercapnia) or a

decrease in arterial oxygen tension (hypoxemia).

• In “length-tension inappropriateness”, patients

experience respiration as being mechanically

insufficient.77 In the body, the relationship

between the actual change in respiratory muscle

length and muscle strength is constantly being

evaluated in terms of expected changes in length.

17


V-03/2003/US

If the length change is smaller than expected, the

person experiences dyspnea. This mechanism is

especially important when an extra demand is

placed on the respiratory apparatus.

• Psychosocial factors: emotional and situational

factors can also be associated with the sensation

of dyspnea.78

Fatigue, respiratory muscle weakness, and the fact

that the minute ventilation in COPD patients is high

all contribute to sensations of breathlessness. When

the minute ventilation is high, every increase in the

ventilation rate is a relatively large increase, which

leads to a proportionally large increase in dyspnea.79

Dyspnea seems to be affected more by repetitive

movements of the upper extremities.80 This may be

explained by the fact that these movements reduce

the ability of the upper chest muscles to contribute to

respiration. Unilateral arm movements involve less

load for the patient than bilateral movements.

Malnutrition

An underweight condition (i.e., a weight under 90%

of the ideal weight) is common in patients with

COPD.35,75,82 Its prevalence increases as the degree of

bronchial obstruction increases.35,75 The muscular

strength of respiratory and skeletal muscles is less in

patients who are underweight than in those with a

normal weight.62,83 Gray-Donald et al.64 reported

that patients who are underweight have a lower

maximum exercise capacity but that the condition

has no impact on submaximal exercise capacity or

dyspnea. In patients with COPD, fat-free body mass is a

better indicator of respiratory and skeletal muscle

strength than body weight82,84 and is a significant

determinant of exercise tolerance.75 A reduction in

fat-free body mass is associated with lower values for

respiratory and peripheral muscular strength.82 In

one group of randomly selected COPD patients (mean

FEV1, 53%), 14% were found to have reduced fat-free

body mass and reduced body weight, and 7% were

found to have only one of the two.82 Here again,

there is a need for communication between the

practitioners of different disciplines because

nutritional interventions in underweight patients can

increase respiratory and peripheral muscle

strength85,86 and improve exercise capacity.86

Diagnosis

The methodical provision of physical therapy is based

on a problem-solving approach.87 Several stages can

be distinguished in this process. The starting point is

referral by a primary care physician or medical

specialist and the patient’s reasons for seeking

medical care. The next stage is history-taking, which

is followed by an examination of the patient and

drawing conclusions, or making a physical therapy

diagnosis. In assessing the patient’s needs, the

physical therapist must determine whether physical

therapy would be helpful. If so, the therapist draws

up a treatment plan, which is periodically evaluated

during the course of treatment and after treatment

ends. The last stage is concluding treatment and

reporting back to the referring physician.88,89

Referral

The physical therapist must have all the relevant

medical and psychosocial data before the patient is

examined and, if necessary, treated. These data guide

the therapeutic approach and help the physical

therapist analyze the patient’s health problems,

interpret the examination results, and formulate

realistic and attainable treatment goals. An

understanding of the severity of the condition and its

prognosis is important for making an accurate

assessment of the results of physical therapy.

Relevant medical data includes data from pulmonary

function tests and, if the physical therapist wants to

improve the patient’s exercise capacity, an

incremental exercise test at the patient’s maximum

exercise rate. According to Cambach et al.45 certain

patients should be treated in special COPD facilities:

those whose arterial oxygen tension (PaO2) is lower

than 8.6 kPa (65 mmHg) and those whose arterial

carbon dioxide tension (PaCO2) is higher than 6.0

kPa (45 mmHg). at rest or during exercise.

History-taking

Details of the information sought and the questions

asked during history-taking are presented in Table 15.

18


V-03/2003/US

19


V-03/2003/US

Noting the patient’s symptoms and current condition:

• reasons for referral; medical referral data (nature of obstruction: chronic bronchitis or emphysema);

• patient’s needs. How does the patient experience the consequences of COPD? What are the patient’s

expectations of treatment (physical therapy)?

• social data (family composition, occupation, family history);

• effects of the condition on emotional functioning;

• Which medications is the patient using and is he or she knowledgeable about their use?

Are there any signs of impaired mucus clearance?

• Does the patient cough? If so, is coughing productive and effective?

• Is there increased sputum secretion? If so, how much? What is the color and consistency of the sputum?

• Is there a relationship between sputum production and body posture, activity or medication use?

• Is the patient familiar with mobilization and expectoration techniques?

• Does mucus retention have any negative effects (e.g., exacerbations, recurrent infection, or fatigue)?

Are there any indications of reduced exercise capacity due to COPD?

• What is the patient’s current level of activity and has it changed as a result of the disorder?

• What is the reason for and the extent of any reduction in exercise capacity?

• Does dyspnea occur? If so, when?

Quality of life questionnaire note 1

Are there any other symptoms?

• hypoxia, hypoxemia, insomnia, morning headaches, or difficulty concentrating?

• Are there any complaints associated with respiratory movement (e.g., restricted movement, pain or

stiffness)?

• Is there any pain associated with deep breathing or coughing?

• Is there cardiac decompensation?

Recording the natural course of the symptoms and condition:

• brief summary of the onset and course of symptoms;

• notes on therapy, medication, primary care physician or specialist, hospitalization, physical therapy, and

other therapies. What were the effects of each type of therapy?

Noting the patient’s load and load-bearing capacity, the causes of symptoms, and any factors that have

influenced or are influencing symptom development:

Evaluating load-bearing capacity:

• Have any traumas occurred or operations taken place?

• Are there any other disorders (e.g., of the locomoter tract or any other tracts)?

• Has body weight decreased despite normal food consumption?

• What is the quality of the patient’s sleep (e.g., problems with falling asleep or staying asleep)?

Evaluating load:

• What demands does the patient’s environment make on him or her?

• What is the patient’s level of activity, including general activities, work and hobbies?

• Are there any aggravating factors (e.g., smoking, hyperreactivity, emotional or behavioral factors, or

factors in the work environment)?

• Which factors reduce symptoms (e.g., resting, specific environmental conditions, or medication use)?

What is the patient’s need for information? note 2

Table 15. Details of history-taking in patients with COPD. The raised figures are references to individual notes in

the appended notes on diagnosis.

Physical examination

The physical examination usually comprises

observation and palpation, since these two processes

often occur at the same time. Palpation is used to

verify the information obtained by observation. The

physical examination is divided into two parts in

order to investigate two specific problems in patients

with COPD. Table 16 describes the details of the

physical examination in patients with impaired

mucus clearance and Table 17 describes the physical

examination in those with impaired exercise capacity.

Analysis

During analysis, the patient’s health problem is

analyzed using referral data and data obtained from

the physical therapy examination. The physical

therapist should be able to determine whether

physical therapy is indicated, or whether the patient

should be referred for consultation elsewhere.

Physical therapy is indicated for patients who,

because of COPD, have impaired mucus clearance,

whose normal daily life activities are limited by

dyspnea, or who have impaired exercise capacity. The

patient should be motivated to undergo treatment

because very active participation is required to

achieve good results. After the completion of

treatment, the patient must be proactive so that the

benefits can be maintained.

Patients can be treated according to these guidelines

if their medication has previously been optimized81

and if the referral data is sufficient. If there are

indications that a patient’s medication is not optimal,

he or she should be referred back to the physician. If

a patient is suffering from disabilities due to reduced

exercise capacity, referral documentation should, if it

is complete, include data from an incremental

exercise test at the patient’s maximum exercise load.

These data are essential for determining the patient’s

exercise limitations so that the appropriate exercise

load can be used and so that the therapist can be sure

there are no contraindications. If the patient does not

satisfy the requirements for participating in exercise

training, the referring physician should be consulted.

Analysis: impaired mucus clearance

Patients with impaired mucus clearance may have

one or more impairments, such as bronchial

obstruction resulting from mucus retention or

airways collapse, or a disorder in mucus transport,

production, composition or clearance.

Systemic factors that can cause or contribute to

impaired mucus clearance include medication use,

malnutrition and other problems such as heart

ailments. These may necessitate consultation with or

treatment by another specialist.

Local factors that can cause or contribute to impaired

mucus clearance must also be taken into


20 51.1001.01.02

Observation:

• evaluation of coughing and huffing techniques. Can the patient cough effectively? Is there pain during

coughing? note 3

• Are there deformities of the thorax (e.g., pectus excavatum, pectus carinatum, or kyphoscoliosis)? note 4

• Is the shape of the abdominal wall abnormal (e.g., due to weakened abdominal musculature)?3

• auscultation and palpation of thoracic wall; note 5

• listening to breath sounds; note 5

• Does airways collapse occur? note 3

• assessing the quantity, consistency and appearance of mucus.

Movement testing:

• How well does the abdominal musculature function (i.e., strength and endurance)? note 3

Other measurements:

• peak expiratory flow. note 6

Table 16. Details of the physical examination in patients with impaired mucus clearance. The raised figures are

references to individual notes in the appended notes on diagnosis.

21


V-03/2003/US

General impression: note 7

• general impression (e.g. movement speed, movement effort, and presence of trunk rotation);

• Is the patient’s preferred position to lean forward when seated or to support their arms?

• Is cyanosis present (color of the face and lips)?

• Is there muscle atrophy or peripheral edema? Is the skin cyanotic, hydrated or trophic?

• Does breathing at rest take visible effort (e.g., nasal flaring or spontaneous pursed-lips breathing)?

• Does the patient speak with a nasal voice or must speech be interrupted frequently?

• Are breath sounds audible?

The position and shape of the thorax: note 8

• Is the thorax in a position normally characteristic of inspiration? note 9

• Are there deformities of the thorax (e.g., pectus excavatum, pectus carinatum, or kyphoscoliosis)?

• Is the shape of the abdominal wall abnormal (e.g., due to obesity or weakened abdominal musculature)?

• Is the shape or position of the lumbar spine, thoracic spine or cervical spine abnormal?

• What is the posture of the shoulder girdle (i.e., shoulder height, protracted position)?

Respiration and respiratory movement: note 10

• Is the respiration rate or depth of breathing abnormal?

• How does the abdominal wall move during inspiration and expiration (i.e., direction and timing)?

• Are the actions of the accessory respiratory muscles abnormal during inspiration and expiration at rest?

• Are the actions of the abdominal muscles abnormal during inspiration and expiration at rest?

• Are there signs of tracheal tug during inspiration?

• Is the infraclavicular or supraclavicular fossa visibly drawn in during inspiration?

• How does the chest move during inspiration and expiration?

• Is the thorax or sternum lifted in an exaggerated way at the beginning of inspiration (i.e., pump-handle

movement)?

• How do the lower ribs move during inspiration (e.g., Hoover’s sign or bucket-handle movement)?

• Are any thoracic excursions asymmetrical?

Movement: note 11

• How is the patient’s functional muscle strength during movement from a supine to a sitting position,

and from a sitting to a standing position?

• How well do the respiratory muscles function (i.e., strength and endurance)?

• How well does the abdominal musculature function (i.e., strength and endurance)?

• other muscle strength tests (e.g., of the quadriceps muscles);

• How is the patient’s balance?

Other measurements:

• peak expiratory flow.note 6

Measurement of exercise capacity: note 12

• walking test; note 13

• cycle ergometer test;

• oxygen saturation (e.g., using a pulse oximeter); note 14

• dyspnea (e.g., using Borg scale score).15

Table 17. Details of the physical examination in patients with impaired exercise capacity. The raised figures are

references to individual notes in the appended notes on diagnosis.

consideration when drawing up a treatment plan and

evaluating treatment. Examples of such factors are

increased mucus viscosity, pulmonary function

limitations, bronchial obstruction, and poor

functioning of respiratory muscles, including the

abdominal muscles. For instance, patients with

purulent sputum may need to be treated more

frequently. Measuring mucus viscosity helps in

assessing how difficult it is for patients to cough up

sputum.

Analysis: impaired exercise capacity

Patients with impaired exercise capacity may be

affected by reduced general physical stamina, or by

respiratory muscle function or gas exchange

disorders, and by feelings of dyspnea. These patients

may also experience disabilities in their mobility and

on their ability to carry out personal hygiene,

housework, occupational, educational or leisure

activities, among other things.

Systemic factors that can cause or contribute to

impaired exercise capacity include medication use,

malnutrition, the presence of other complaints, and a

reduced activity level. These may necessitate

consultation with or treatment by another specialist.

Local factors that can cause or contribute to impaired

exercise capacity include pulmonary function

limitations, oxygen transport disorders, and poor

respiratory muscle function.

Treatment plan

After analysis, a treatment plan can be drawn up for

the individual patient. Treatment plans are tools for

structuring, monitoring and evaluating treatment.

The treatment plan records treatment goals, the

procedures to be used in treatment, the treatment

strategy, and the patient’s and physical therapist’s

individual responsibilities.

The treatment plan can be divided into two phases.

The aim of the first phase is to minimize or eliminate

impairments in the musculoskeletal system. For

patients with COPD, this means that the load on the

muscles controlling breathing should be reduced as

much as possible by reducing airway obstruction (i.e.,

by improving mucus clearance) and by reducing the

patient’s habitual expansion of the thorax as much as

possible from a position that is characteristic of

inspiration. Airway collapse must be prevented as far

as possible. In the second phase, the aim is to

normalize respiratory movement. For patients with

COPD, this involves adjusting respiratory movement

by optimizing the contribution of the respiratory

system’s compensatory mechanisms.

In both phases, the patient’s load-bearing capacity

can be increased. Increasing specific load-bearing

capacity partly involves improving the strength and

endurance of respiratory muscles. Increasing general

load-bearing capacity involves improving physical

stamina. The results of the physical therapy

diagnostic process determine the different emphases

in treatment.

Therapy

The therapeutic approach adopted is, in part, based

on systematic reviews of the scientific literature. The

literature considered for these reviews was collected

from the MEDLINE database and from databases of

the Dutch Institute of Allied Health Professions (NPi),

including a physical therapy index, a rehabilitation

index and an occupational therapy index. The

collected items were supplemented by scrutinizing

reference lists and by receiving additional material

from members of the steering group. Studies were

only included if they involved randomized clinical

trials on (a) the effects of physical therapy on mucus

clearance, (b) the effects of exercise training as part of

pulmonary rehabilitation in patients with COPD, or (c)

the effects of inspiratory muscle training in patients

with COPD. Each trial was evaluated on its

methodological quality by two independent reviewers

using 10 predefined criteria.90,91 These criteria were

based on generally accepted principles of scientific

research.92–94 As no more than one point was

awarded for each criterion, the highest possible score

for any trial was 10. A trial was considered to be of a

sufficiently high quality methodologically if it scored

more than five points. The conclusions drawn about

therapy are based on such high-quality trials.

Improving mucus clearance

Physical therapy employs a variety of methods for

improving mucus clearance. The following

22


V-03/2003/US

techniques will be described sequentially: coughing

or forced expiration; postural drainage; exercise; chest

percussion and mechanical vibration; positive

expiratory pressure; the Flutter device; and autogenic

drainage. A systematic review of the efficacy of these

procedures was carried out. Inclusion criteria were:

• a randomized clinical trial was involved;

• the results concerned only one group of COPD or

cystic fibrosis patients;

• the patients underwent a physical therapy

intervention aimed at improving mucus clearance;

and

• the study outcome measures were relevant to

mucus clearance.

Coughing or forced expiration

Mechanism of action

The expiratory airflow rate is high during coughing

and forced expiration, thereby assisting mucus

transport from peripheral to central airways.53,95

Initially during coughing, high intrapulmonary

pressure is built up when the glottis is closed;

thereafter, the expiratory airflow is high when the

glottis opens. Huffing, in contrast, involves forced

expiratory airflow with an open glottis, which means

that the intrapulmonary pressure is much lower.96 If

the expiratory airflow is to be sufficient for

transporting mucus, a high flow velocity of, at least, 1

m/s (greater than 2.5 m/s is better) is needed.53

Furthermore, the thickness of the mucus layer is also

important. Coughing and huffing are more effective

when the mucus layer is thick.53

During forced expiration and coughing, dynamic

compression of the airways takes place. Dynamic

compression contributes to the development of very

high local airflow velocities in the respiratory tract.

The exact location at which the dynamic

compression caused by expiratory forces takes place

(i.e., the equal pressure point). is dependent on lung

elasticity (or lung volume), bronchial obstruction,

and bronchial stability.97

Mucus transport can be facilitated by varying the

expiratory force and equal pressure point. If there are

signs of airway collapse, however, dynamic

compression must be avoided. By using less force and

starting from a greater lung volume, compression

occurs more centrally and collapse can be, at least

partially, prevented. The advantage of forced

expiration over coughing is that the lung volume and

force can be better controlled.

Evidence supporting mucus clearance by coughing

Multiple controlled trials have shown that coughing

improves mucus transport and, thereby, mucus

clearance.98–100 The study by van der Schans et al.100

found a difference between chronic bronchitis

patients, in whom coughing was effective, and

emphysema patients, in whom the efficacy of

coughing could not be proven. It was suggested that

coughing may be less effective if lung elasticity is

compromised.

The literature also revealed that coughing is more

effective than postural drainage,98,99 but that physical

therapy (described as the combination of breathing

exercises, chest percussion, vibration, and postural

drainage) does not appear to provide any additional

benefits to coughing alone.99

Evidence supporting mucus clearance by forced

expiration (including postural drainage)

Van der Schans et al.100 report that forced expiration

techniques have positive effects in patients with

chronic bronchitis but not in those with emphysema.

The reason could be, as noted above, that forced

expiration may be less effective when the elasticity of

the lungs is compromised. When used in

combination with postural drainage, forced

expiration is effective in clearing mucus.101–103

However, it is not possible to compare the efficacy of

forced expiration techniques with that of other

procedures on the basis of evidence from the

scientific literature because the forms of the different

interventions used were highly variable as were the

types of intervention being compared.104,105

Postural drainage

Mechanism of action

In healthy individuals, the effect of gravity on mucus

clearance is negligible. This changes, however, when

there are alterations in viscoelastic properties, ciliated

epithelium function, the quantity of mucus, and the

thickness of the periciliary layer.106

23


V-03/2003/US

Postural drainage techniques use gravity to promote

mucus transport. In practice, a particular posture is

held for a minimum of 20 minutes, with the relevant

bronchus being held vertically. It is essential that the

location of the mucus is appropriate for the posture

being held. Nine specific postures for draining the

large bronchi have been reported.107

Evidence

The efficacy of postural drainage has not been

unequivocally substantiated by literature findings.

Rossman et al.99 reported positive results in patients

with cystic fibrosis, whereas Oldenburg et al.98

showed negative results in patients with bronchitis.

The effects of postural drainage have been reported to

be inconsistent when it is used in combination with

other procedures.108,109

Exercise

Mechanism of action

Exercise increases expiratory flow velocity, the

respiratory minute volume, and sympathetic nervous

system activity. These mechanisms increase the

ciliary beat frequency, reduce mucus viscosity and,

thus, increase mucus transport.110

Evidence

The only explanatory study on the efficacy of exercise

that was of sufficiently high methodological quality

showed positive results. Exercise was found to

increase bronchial mucus transport.98 The authors of

that study also demonstrated that coughing brings

about better mucus clearance than exercise. In a

pragmatic study, no differences were found when

treatment involving exercise plus forced expiration

was compared with other interventions.108

Chest percussion and vibration

Mechanism of action

The physical vibration caused by chest percussion or

a mechanical vibrator is transferred to lung tissue and

to the respiratory tract. Mucus is loosened by the

vibration and cilia activity is stimulated. The mucus

composition may also by changed by vibration.111,112

In their reviews, Hansen et al.113 and Thomas et al.114

summarized the mechanisms of action of percussion

and vibration. The resulting motion can reduce

mucus viscosity, stimulate coughing, or, by a

resonance effect, reinforce ciliary movement.112 In

addition, Thomas et al.114 noted improvements in

ciliary function and changed mucus composition. A

percussion frequency of 25–35 Hz is optimal for

mucus transport, but is not achievable manually.115

After reviewing the literature, Thomas et al.114

concluded that the optimal frequency of vibration for

improving mucociliary clearance had not been clearly

defined but that it is under 60 Hz.

Evidence supporting mucus clearance by percussion

The evidence that percussion improves mucus

clearance is limited. The literature review did not

contain any explanatory studies of sufficiently high

methodological quality that proved percussion was

effective. Therefore, it is not possible to say whether

percussion is more effective than giving no

treatment. However, it appears that percussion given

in addition to postural drainage offers no benefits

over postural drainage alone99 nor over physical

therapy alone (defined as postural drainage plus

coughing).116

Evidence supporting mucus clearance by vibration

The only explanatory study on the efficacy of

vibration that was of sufficiently high

methodological quality gave negative results. No

difference was demonstrated between periods in

which vibration was applied and control periods.117

Positive expiratory pressure

Mechanism of action

Before mucus can be cleared from the small airways

by coughing or forced expiration, it must be moved

to a more central part of the respiratory tract. This

can be accomplished by using a positive expiratory

pressure mask or mouthpiece to give an expiratory

pressure of 10–20 cmH2O (centimeters of water).

Increasing the functional residual capacity of the

lung enables the airways to remain open during

expiration.118 Applying positive expiratory pressure

raises the pressure gradient between open and closed

alveoli, which reduces resistance in collateral and

small airways.119,120 This process encourages

collateral ventilation, enabling air to collect distally

behind the mucus. Mucus is then moved to the

central respiratory tract.

24


V-03/2003/US

Evidence

The application of positive expiratory pressure

increases the functional residual capacity of the lung,

but this has no effect on mucus clearance. The

efficacy of positive expiratory pressure used alone

cannot be demonstrated.121 Several trials have shown

that positive expiratory pressure used in combination

with forced expiration, or coughing or huffing, does

lead to improved mucus clearance.102–104 However,

these trials do not indicate the magnitude of the

contribution of positive expiratory pressure. Because

of variability in the nature of the interventions used

and in the types of interventions being compared in

different studies, it is not possible to say how effective

positive expiratory pressure is in comparison to other

types of therapy, whether used alone or in

combination.105,108,109

Flutter device

Mechanism of action

The Flutter device uses a combination of positive

expiratory pressure and vibration or oscillation

applied through the mouth. An expiratory pressure of

5–35 cmH2O is achieved by asking the patient to hold

a small ball in the air by blowing. The movement of

the ball causes an oscillatory movement at a

frequency of 8–26 Hz.122 In this form of treatment,

respiratory tract dilatation caused by increased

expiratory pressure and airway vibration are thought

to improve mucus transport.52

Evidence

The literature review found two trials that examined

the effects of the Flutter device used in addition to or

instead of physical therapy.123,124 Both trials are of

low methodological quality and, furthermore, show

inconsistent results. The efficacy of the Flutter device

cannot, therefore, be substantiated.

Autogenic drainage

Mechanism of action

Autogenic drainage is a method in which patients

learn how to promote mucus drainage by themselves.

Controlled breathing techniques in which the

frequency and depth of breathing are varied are used

to achieve the highest possible airflow at different

levels of bronchial tree. In other words, a balance is

sought between expiratory flow, intrabronchial

pressure and bronchial wall stability. The hypothesis

is that mucus is mobilized when the patient breathes

at a low expiratory flow rate with the lung volume

lying between the functional residual capacity and

the residual volume. Thereafter, mucus is transported

to larger airways by the increase in the tidal volume.

Finally, mucus is expectorated by forced expiration,

starting with a low lung volume.125

Evidence

Miller et al.126 found no difference in mucus

expectoration between patients who used autogenic

drainage and those who used physical therapy (i.e.,

an active cycle of breathing techniques). However,

mucus clearance starts more quickly with autogenic

drainage.

Effect of physical exercise as part of pulmonary

rehabilitation

A total of 18 trials on the efficacy of physical exercise

as part of pulmonary rehabilitation in patients with

COPD were reviewed. Eleven trials were of sufficiently

high methodological quality. Physical exercise was

found to have a positive effect on stamina and

quality of life in COPD patients. The effects of exercise

on walking distance, maximum and submaximal

exercise capacity, and quality of life are described

sequentially below.

Seven trials studied the effect of exercise as part of

pulmonary rehabilitation on walking distance127–133

and on maximum exercise capacity.127–129,132,134–136

Five of the seven found a positive effect on walking

distance127–131 and four found a positive effect on

maximum exercise capacity.127,129,134,135

Exercise used as part of pulmonary rehabilitation has

also been shown to have a positive effect on

submaximal exercise capacity.130–134,137 However,

Reid and Warren136 and Busch and McClements135

failed to demonstrate any significant effect on

submaximal exercise endurance. In addition,

improvements in exercise capacity, or maximum

exercise capacity, appeared to occur in patients with

severe forms of COPD (i.e., with an FEV1 of between

35–49% of that predicted).129–131,135,136,138

In addition to improving exercise tolerance,

25


V-03/2003/US

rehabilitation programs can also lead to decreased

dyspnea at rest, as assessed by the Chronic

Respiratory Disease Questionnaire131–133,138 and

during exercise.129,134,137 However, Busch and

McClements135 found no resulting difference in the

sensation of dyspnea.

Research using different measures on the Chronic

Respiratory Disease Questionnaire have given the

following results. Of four trials that used the measure

of fatigue,131–133,138 two showed that exercise as part

of pulmonary rehabilitation reduces fatigue.132,133 Of

four trials that used the measure of emotion from this

questionnaire,131–133,138 two showed positive

results.131,138 In addition, all four trials that used the

measure of mastery131–133,138 showed that exercise

training as part of pulmonary rehabilitation had a

positive effect. A recent meta-analysis has confirmed

the positive effects of pulmonary rehabilitation on

exercise capacity, dyspnea and quality of life.139

Content of rehabilitation programs

Research by Ries et al.134 showed that physical

exercise is an essential part of rehabilitation.

Providing education alone is not enough to improve

exercise capacity. Most rehabilitation programs offer

walking, with or without the use of a treadmill, or

cycling as methods for improving exercise tolerance.

In some trials, climbing stairs135,137 or rowing130 were

used as interventions. Two studies found that

training the upper extremities improves the strength

and endurance of the relevant muscle groups in

patients with COPD.140,141 Both trials, however, are of

low methodological quality.

Exercise program duration, frequency and

intensity

Literature studies reveal that the duration of exercise

programs used varies from six weeks137 to six

months.131 Positive effects are demonstrable after six

weeks or more. The duration of most programs is

between 8–12 weeks. The effect of training reaches a

plateau within 3–6 months.

The frequency with which patients exercise,

including training and practice sessions, ranges from,

at least, twice a week129,137 to five times a week, or

daily.134,135,138 Positive effects are achievable with

programs that involve twice weekly or more frequent

sessions. Recently, it has been demonstrated that

patients with COPD can cope with high-intensity

exercise.134,142 One study indicated that training at a

high load produces better results than training at a

low load.143 This study was conducted on a group of

patients with a moderate degree of bronchial

obstruction. Maltais et al.144 studied the effects of

high-intensity exercises on patients with moderate or

severe bronchial obstruction. They found that most

patients cannot sustain a high load (i.e., 80% of

maximum load). However, significant improvements

in exercise capacity and a physiological adaptation to

exercise occurred.

26


V-03/2003/US

Outcome measure Trials showing a positive (+) or negative (-) effect on the

outcome measure

Walking distance +(127) +(128) +(129) +(130) +(131) -(132) -(133)

Maximum exercise capacity +(134) +(127) +(129) +(135) -(128) -(132) -(136)

Exercise endurance +(134) +(132) +(133) +(130) +(131) +(137) -(136) -(135)

CRDQ dyspnea measure +(138) +(131) +(133) +(132) -(135)

CRDQ fatigue measure +(132) +(133) -(131) -(138)

CRDQ emotion measure +(138) +(131) -(133) -(132)

CRDQ mastery measure +(138) +(132) +(131) +(133)

Note: The trials reported in references 129 and 132 involved an intragroup comparison within the

experimental group.

Table 18. Summary of the results of randomized clinical trials of sufficiently high methodological quality on the

effects of exercise training as part of pulmonary rehabilitation. CRDQ = Chronic Respiratory Disease Questionnaire.

Follow-up

The importance of follow-up after a rehabilitation

program is clearly demonstrated by data from

Wijkstra et al.42 The researchers found that exercise

capacity tended to decrease over time, but that the

benefits could be maintained by arranging follow-

ups. Ries et al.134 followed patients after completion

of a rehabilitation program or an educational

program. Soon after the programs were completed,

there were significant differences between the two

groups, with the rehabilitation group showing more

positive results. Over the course of time, however,

these differences became less marked. In one study,

six years after rehabilitation, the survival rate in

patients who followed a rehabilitation program was

higher than in those who did not, at 67% compared

to 56%, respectively.134 The difference was not

statistically significant, however.

Effects of inspiratory muscle training (IMT)

Studies were included in the literature review if they

involved randomized clinical trials in which COPD

patients underwent respiratory muscle training to

improve the strength and endurance of respiratory

muscles. If resistance loading was involved, pressure

at the mouth had to have been measured. As the

guidelines state that training intensity should also be

defined, it was later decided to exclude trials in which

training intensity was not explicitly

described.136,145,146 Studies that involved training

with normocapnic hyperpnea were excluded147–149

because this training regimen is not practically

applicable. After applying these selection criteria, 10

trials remained for inclusion in the systematic review.

All were of sufficiently high methodological quality.

Effects of inspiratory muscle training on the

strength and endurance of inspiratory muscles

In COPD patients, genuine respiratory muscle training

leads to a significant increase in respiratory muscle

strength compared with placebo respiratory muscle

training. Increased endurance and reduced dyspnea

have also been reported.150

High-resistance respiratory muscle training produces

a greater increase in strength and endurance from

baseline than low-resistance training.151–155 In two of

the five trials considered, respiratory muscle strength

was different from that in the control group.151,153

However, Lisboa et al.,155 Harver et al.156 and Preusser

et al.152 found no difference in respiratory muscle

strength between the group that trained at a high

load and the group that trained at a low load. In

addition, Larson et al.151 and Preusser et al.152 found

no difference between the two groups in terms of

respiratory muscle endurance.

General effects of inspiratory muscle training

Two of the above five trials examined the effect of

respiratory muscle training on dyspnea.154,155 Both

found that respiratory muscle training reduces

dyspnea. Three of the five trials examined the effects

of respiratory muscle training on walking

distance.151,152,155 All three found that walking

distance had increased in the group that trained at a

high load. In addition, Preusser et al.’s study152 found

that walking distance in the group that trained at a

low load had also increased. Only Larson et al.’s

study151 found a significant difference between the

two groups.

Inspiratory muscle training combined with

exercise training

Four trials investigated the effect of adding

respiratory muscle training to exercise training by

comparing groups that received both with groups

that received exercise training alone.58,128,130,156 In all

trials, the groups that received respiratory muscle

training showed increased respiratory muscle

strength and endurance compared to baseline. This

was not seen in Berry et al.’s study128 because no

baseline values were given.

Two of these four studies showed that respiratory

muscle training provided additional gains in terms of

respiratory muscle strength and diaphragm

fatigability.58,156 Weiner et al.130 did not make any

between group comparisons, and Berry et al.128 found

no difference between the two groups.

Three of the four studies examined the additional

benefits of respiratory muscle training on walking

distance and maximum exercise capacity. Two trials

showed that respiratory muscle training gave

additional benefits,58,130 whereas another study

found that walking distance was improved by

27


V-03/2003/US

exercise training but not by respiratory muscle

training.128

The only study that investigated the additional

effects of respiratory muscle training on dyspnea

found no difference between the two training

groups.128 Moreover, Dekhuijzen et al.58 failed to

show that respiratory muscle training offered any

additional benefit in terms of performing normal

daily activities or of emotional functioning.

The results of all these studies are summarized in

Table 19.

Exercise load, duration and frequency

Preusser et al.152 found that a training intensity of

22% PImax resulted in improved respiratory muscle

endurance and increased walking distance, but

produced no difference in respiratory muscle

strength. Larson et al.151 found no significant change

in respiratory muscle strength or endurance or in

walking distance at a training intensity of 15%

PImax. Lisboa et al.155 found an increase in strength

at a training intensity of 10% PImax. In contrast,

Heydra et al.153 found no increase in strength at a

training load of 10% PImax and Larson et al.151

found no increase in strength at a training load of

15% PImax. The literature review, therefore, found no

consistent evidence about which training intensity

results in training effects nor did it show that a

higher load leads to better results.

Literature findings on the optimum duration and

frequency of training are inconsistent. Different

studies report training periods varying from eight

weeks150,151,154,156 to six months.130 However, most

trials used a training duration in the range of 8–12

weeks.

The frequency of respiratory muscle training reported

in the selected literature varies from four 15-minute

sessions a day150 to three 15-minute sessions a

week.130 However, most trials employed a frequency

of two 15-minute sessions a day.

Since no consistent conclusions on exercise load,

duration and frequency can be derived from the

literature review, following the example of the

European Respiratory Society, it is recommended that

respiratory muscle training takes place five to seven

28


V-03/2003/US

Outcome measure Explanatory] trials Pragmatic trials: Pragmatic trials:

high load versus low load respiratory muscle training

with or without exercise

Respiratory muscle strength* +(150) +(151) +(153) -(152) +(58) +(156) +(130) –(128)

–(154) –(155)

Respiratory muscle endurance* +(150) +(153) –(151) –(152) +(58) +(156) +(130) –(128)

Dyspnea +(150) –(128) +(154) +(155)

Walking distance +(151) –(155) –(152) +(58) +(130) –(128)

Exercise capacity** –(155) +(130) +(156)

Performance of normal daily –(58)

activities and emotional

functioning

* includes strength or diaphragm fatigability;

** (sub)maximum exercise capacity (including maximum oxygen volume consumption rate, VO2max); + =

there is a significant difference between the intervention and control groups in favor of the intervention

group; – = there is no significant difference between the two groups.

Note: The study of respiratory muscle strength and endurance carried out by Weiner et al.130 involved an

between group comparison within the experimental group.

Table 19. Summary of the results of randomized clinical trials of sufficiently high methodological quality on the

effect of respiratory muscle training, listed in terms of outcome measures.

days a week for two 15-minute sessions per day for a

minimal training duration of eight weeks. The

training load should be between 30–40% PImax157

Training method

Different training methods place different loads on

the respiratory muscles. It is possible to customize the

method for each individual on the basis of the

magnitude of pressure or flow, or a combination of

the two.158 If resistance loading is used, pressure at

the mouth will need to be monitored in order to be

certain that a specific load is being applied. A change

in breathing strategy, in particular one involving the

use of slow deep breathing, can reduce the actual load

on the respiratory muscles.159 By consensus, the

steering group recommends that the ratio of

inspiration time to expiration time should be

maintained at 3:5.

The threshold training method has been shown to be

a reliable and reproducible method of loading the

respiratory muscles in patients with COPD.160

Decreasing dyspnea

Active expiration

When respiratory demand increases in healthy

people, the abdominal muscles automatically begin

to take up some of the load.161 In patients with COPD,

the abdominal muscles contribute to breathing even

at rest. This almost exclusively involves the transverse

abdominal muscle.162 Tensing the abdominal muscles

during expiration improves the position of the

diaphragm, enabling it to deliver more force.

Reybrouck et al.163 compared the effects of active

expiration using myofeedback from the abdominal

muscles with active expiration without such

feedback. The patient group who used myofeedback

showed a significantly greater decrease in functional

residual capacity and an increase in PImax.

Reducing the respiratory rate

Breathing at a low frequency at rest results in

improved alveolar ventilation and better arterial

blood gas concentrations. However, during exercise,

low-frequency breathing does not significantly

improve gas exchange and the respiratory minute

volume is significantly reduced.164

Body posture

Adopting a particular body posture can lengthen the

diaphragm, enabling it to provide more force and to

contribute more to respiration. The study carried out

by Sharp et al.165 supports this observation. They

found that, in patients who benefit from leaning

forward, electromyographic activity in the inspiratory

accessory muscles increases significantly when they

stand up straight or sit. In contrast, therefore, leaning

forward reduces electromyographic activity in the

accessory muscles. The trials conducted by Druz and

Sharp166 and O’Neill and McCarthy167 point to the

same conclusion: that leaning forward improves the

function of the diaphragm.

Pursed-lips breathing

Pursed-lips breathing involves exhaling steadily

through slightly pursed lips. This action counteracts

dynamic compression of the respiratory tract such

that functional residual capacity decreases and

inspiratory capacity increases. In addition, pursed-lips

breathing slows the respiratory rate and increases

tidal volume.79,168,169 Not every patient benefits from

this technique. The effects of pursed-lips breathing

(i.e., decreased respiratory rate and increased tidal

volume) are more significant in patients who benefit

from pursed-lips breathing.79 Moreover, pursed-lips

breathing at rest improves blood gas

concentrations.79,168,169 These effects have not been

observed during exercise.79 Pursed-lips breathing at

rest can reduce dyspnea. The mechanism of action is

not yet clear.

Diaphragmatic breathing

Diaphragmatic breathing is wrongly thought to be an

effective way of breathing. Gosselink et al.170 found

that diaphragmatic breathing in severe COPD patients

results in poorer coordination of respiratory

movement and decreased mechanical efficiency of

the diaphragm. There is also a tendency for dyspnea

to increase.

Habituation

The mechanisms causing habituation are not yet

understood. Various trials have shown that exercise

can reduce dyspnea but physiological training does

not appear to have an effect.171,172 Rosser and Guz173

have suggested that psychological factors may

29


V-03/2003/US

explain the reduction in dyspnea. Another study of

the importance of psychological factors showed that

dyspnea can be reduced if training occurs in a

familiar environment174 and if distracting stimuli

such as music are present during exercise.175 These

effects may occur because cognitive and contextual

factors play a role in dyspnea.

Another mechanism could be desensitization. In

desensitization, psychological or physiological factors

may lead to reduced awareness of dyspneic stimuli or

to reduced sensitivity of peripheral or central

receptors, or both.

Improving compliance with therapy

Kanters176 carried out a literature review of the

efficacy of patient education. He concluded that

patient education does result in greater compliance

with therapy in short-term disorders, but that

ensuring compliance with therapy in chronic

disorders requires continuous attention: “Patient

education cannot change the somatic basis of chronic

bronchitis or pulmonary emphysema at all. What

does occur is that the patient gains a greater grasp of

and copes more wisely with his disease”.176

Van der Burgt and Verhulst177 carried out an

overview of all the education models used in health

education and translated them into a model of

patient education for use in allied health care

practice. In so doing, they integrated the Attitude,

Social Influence and Personal Efficacy determinant

model with Hoenen et al.’s step-by-step approach to

providing information.178 The Attitude, Social

Influence and Personal Efficacy determinant model is

based upon the assumption that willingness to

change behavior is determined by a combination of

the patient’s attitude (how the individual perceives

behavioral change), social influences (how others see

behavioral change) and the patient’s perception of his

own efficacy, his self-efficacy (whether the patient

thinks it will work or not). The step-by-step approach

to providing information proposed by Hoenen et

al.178 distinguishes between the stages of openness,

understanding, willingness and doing. With allied

health care practice in mind, van der Burgt and

Verhulst added two extra phases: ability and

persistence. To do justice to the patient’s

individuality, another phase, designated ‘the person’,

was added to the model, as described below. Van der

Burgt and Verhulst177 regard patient information as a

process in which behavioral modification is the final

step. This final step cannot be taken until the

previous stages are complete. The six stages must be

completed sequentially. See Table 20.

In addition, during all stages of the educational

process, it is important to take individual

characteristics of the patient into account, such as his

or her:

• locus of control; To what extent does the patient

believe that he or she can influence the course of

his or her life?

• attribution; What factors does the patient regard

as influencing the course of his or her life?

• coping styles; How does the patient react to

significant events in his or her life?

• emotional state; Is the patient unable to accept

new information because of his or her emotional

state? The answer to this question may also

determine how the patient handles his or her

disease and its treatment.

Knibbe and Wams179)describe a system for increasing

compliance with therapy. It differentiates between

short-term and long-term compliance. To achieve

long-term therapeutic compliance, a great deal of

attention must be paid to evaluating the advantages

and disadvantages of therapy and to the individual’s

sense of their own effectiveness. The patient’s

perception of the advantages and disadvantages of

therapy can be influenced by logical argument. The

patient’s sense of individual effectiveness can be

increased by helping him or her to feel that he or she

is capable of performing the behavior, i.e., that he or

she has mastery over the situation.

Education plan

The physical therapy treatment plan must include an

education plan, in which subgoals are formulated for

each stage. The education plan can be seen as part of

a methodical approach to patient management. It

can begin during history-taking with an analysis of

the patient’s need for information: What does the

patient know about his or her disorder and about the

medications he or she will use? How efficient is the

30


V-03/2003/US

method used for administering the medication and

does the patient know how it can be improved? What

are the patient’s and his or her partner’s expectations

of treatment? At every stage, it is important to pay

attention to any problems the patient is

experiencing. By adopting this approach, information

about the possible causes of any problems in

complying with therapy can be obtained.

Dekkers180 subdivides patient education into four

categories: information, instruction, education and

guidance. This classification is hierarchical in that

activities in the category of information require the

least intervention whereas those in the category of

guidance require the most.

• Information: providing the patient with factual

information about the disease, its treatment, and

medical care.

• Instruction: providing specific guidelines or

recommendations for patients to enable them to

assist the treatment process.

• Education: providing an explanation of the

disease and its treatment in such a way that the

patient understands the background to and

consequences of the condition and appreciates

what he or she can do to keep the disease under

control. Self-care skills should be practiced, if

necessary.

• Guidance: supporting the patient emotionally so

that he or she can cope with and come to terms

with the disease and its effects to the greatest

extent possible.

31


V-03/2003/US

1. Openness

In patient education, the physical therapist must take into account the patient’s perceptions, expectations,

questions and concerns. Significant questions are: What is the patient most concerned about? What

preoccupations prevent the patient from being open to information about behavioral modification?

2. Understanding

Information must be presented in such a way that the patient understands it and can remember it. The

important points here are: not to present too much information at one time, to decide what information

must be presented first and what can be given later, and to repeat the message (if necessary, in another way)

and to explain it using educational aids, such as leaflets or videos. The physical therapist should check

whether the patient has actually understood the information.

3. Willingness

The physical therapist notes the factors that make the patient unwilling to act. The important questions

here are: In what way does the patient benefit from exercise? Is the patient encouraged or discouraged by

people in his or her close environment? Does the patient feel that he or she can influence the situation? The

physical therapist provides support and information on alternative courses of action. Achievable goals are

set.

4. Ability

The patient must be able to carry out the desired behavior. The essential functions and skills must be

practiced. It is important to find out what practical problems the patient expects and to explore with the

patient how these problems can be solved.

5. Doing

This stage includes implementation of the new behavior. The physical therapist makes clear, specific,

attainable agreements with the patient and sets specific goals. If possible, positive feedback is given.

6. Persistence

The patient should continue to carry out the behavior after the end of treatment. During treatment, the

physical therapist must find out from patients whether they thinks they will succeed in continuing. It is

important to find out what discourages and what encourages the patient, and what the short-term and long-

term benefits are. What helps the patient to get back on track after a relapse?

Table 20. The six stages in the process of patient education.

In practice, these four categories overlap. However, it

is important to distinguish between them so that

different goals can be targeted during patient

education. The practical consequences of the

different categories of activity are quite different, as

are the time and educational aids and skills required.

Activities under the category of education involve a

more didactic style and require more teaching aids

than disseminating information. Signs of denial or

non-acceptance indicate that the patient’s greatest

need is for emotional support. If this is the case, the

referring physician should be consulted.

The following subjects must be covered in patient

education:134,181

• medical aspects of the disorder, including the

physiology and pathophysiology of respiration;

• COPD and medication use, including oxygen

therapy;

• medication techniques and personal hygiene;

• healthy eating;

• physical therapy and breathing exercises;

• personal advice on movement; and

• ways to improve social participation.

In a study of the role of patient education in physical

therapy, Sluis182 concluded that it is a vital

component of treatment: information was provided

in 97% of therapy sessions. On the basis of this study,

Sluis made a number of observations:

• little information was given on matters of general

health, health education, and psychosocial

support, even though patients needed it. More

clarity is needed in those subjects that physical

therapists have to communicate.

• most of the information was given in the first two

sessions. The patient education plan should be

designed so that the information can be provided

evenly over the course of treatment. It is possible

for the therapist to work systematically and to pay

attention to all aspects of education without

patients having to receive too much information

at one time;

• two factors that significantly influence

compliance were the obstacles patients

experienced and a lack of positive feedback. To

help counteract these, the exercises and advice

given should be tailored to the individual patient’s

situation. The physical therapist must also

regularly pay attention to the problems

experienced by patients in performing exercises

and in implementing behavioral modification.

The physical therapist should also make greater

use of positive feedback.

In the Netherlands, the (Dutch) National Center for

Medical Information and Health Education (GVO), the

Dutch Asthma Foundation, and COPD nurses can offer

support during the educational process.

Completion of the treatment

At some point during treatment and, necessarily, at

the end of treatment, the referring physician should

be informed about the treatment carried out and its

results.183 Interdisciplinary communication is as

essential part of effective rehabilitation.

After-care

After treatment has been completed, patients must

adopt an active approach to maintain the gains they

have achieved. After-care usually involves regular

exercise. In the Netherlands, the Dutch Asthma

Foundation (Nederlands Asthma Fonds) organizes

athletic groups for individuals with COPD. These

involve participation in specially adapted group

sports and games. The patient’s health status

determines whether participation in an athletic group

is possible. The exclusion criteria are an FEV1 of less

than 1000 ml (or less than 45% of that predicted) or

arterial hypoxemia during exercise. In the

Netherlands, alternative sporting activities are

organized in several cities for patients who cannot

participate in regular COPD athletic groups.

Information about these activities can be obtained

from the Dutch Asthma Foundation.

The legal significance towards the guidelines

Guidelines are no statutory regulations, but they give

insights and recommendations, based on the results

of scientific research, which health care workers must

fulfill to attain quality care. Since the

recommendations are mainly based on the ‘average

patient’, the health care workers have to use their

professional autonomy to deviate from the guidelines

if this the patient’s situation requires this. Whenever

there is a deviation from the guidelines, this has to be

32


V-03/2003/US

augmented and documented.1,2 The responsibility for

the interventions remains with the individual

physical therapist.

Revisions

The KNGF-guidelines are the first development in

clinical questions pertaining to diagnostics, treatment

and prevention for patients with chronic bronchitis

and emphysema. Developments that can improve the

physical therapeutic care of this group of patients,

can change the current insights written in the

guidelines. In the method for developing and

implementing guidelines is indicated that all

guidelines will be revised after three to five years

maximum after the original publication.1,2 This

means that the KNGF, together with the working

group, will decide not later than in the year 2003 if

these guidelines are still accurate. If necessary a new

working group will be installed to revise the

guidelines. The validity of the guidelines expires if

new developments give reasons to start a reversionary

process.

Before the reversionary process, also the Method for

Guideline Development and Implementation will be

updated based on new insights and cooperation

agreements made between the several guideline

developers in The Netherlands. The consensus

products of the Evidence Based Guideline Meeting

(EBRO platform), which are developed under the

auspices of the CBO, will be included in the updated

method. The uniform and transparent methods for

the determination of the amount of evidence and the

derived recommendations for practice are important

improvements.

External financing

These guidelines are subsidized by the Dutch Asthma

Foundation (NAF). The possible interests of the

subsidizer have neither influenced the content of the

guidelines nor the related recommendations.

Acknowledgement

We would like to thank all members of the second

workgroup for their part in the realization of these

KNGF-guidelines. They are: prof. dr. H. Th. M.

Folgering, mrs. prof. dr. D. S. Postma, mrs. E. M. A. L.

Rameckers, mrs. M. Telkamp, dr. J. M. Rooyackers, mr.

Thiadens and drs. Ph. J. van der Wees. Dr. ir. C. P. van

Schayck and drs. W Cambach are thanked for their

valuable contribution to the guidelines.

33


V-03/2003/US

Notes on diagnosis1. One or more questionnaires may be used to

assess quality of life. The Chronic Respiratory

Disease Questionnaire (CRDQ), the St George’s

Respiratory Questionnaire (SGRQ) and the

Medical Psychological Questionnaire for Lung

Diseases (MPQL)186 are useful for the physical

therapist and have been tested for reliability

and validity. The MPQL) is no longer available

and will, therefore, not be discussed further

here. The CRDQ covers the effects of dyspnea on

normal daily activities, emotion, fatigue, and

symptom control.40,185,186 The SGRQ evaluates

symptoms, activities limited by dyspnea, and

the impact of COPD on other factors, such as

work, symptom control, and normal daily

activities.187,188 More information is given in

Chapter 7 of the Dutch project report.189 These

questionnaires are primarily intended to

enable the therapist to gain an impression of

the patient’s quality of life and to describe

treatment. They are not intended to determine

the effects of treatment in individual patients

because they were developed to study groups

and it is not clear how valid they are for

individuals. The SGRQ is freely available for use

(see discussion of measuring instruments in

the guidelines). Answer sheets are required to

use the CRDQ (these can be ordered through the

physical therapy departmental office at the VU

Hospital in Amsterdam, the Netherlands).

2. As far as possible, patients themselves should

determine what information they need. As a

result, the medical practitioner will be better

able to understand the patient’s life, the

patient will find the information more useful,

and he or she will be encouraged to share

responsibility for communication with the

medical practitioner.190 The treatment team

must agree on who is responsible for providing

what information to the patient.

3. Coughing or huffing may be unproductive

because there is: an inadequate expiratory

force due to muscle weakness, pain or

abdominal wall insufficiency; insufficient

inspiratory breathing volume; or

tracheobronchial collapse.14

4. This provides information on where mucus

retention can occur.

5. This provides information on where sputum is

being retained.

6. The peak expiratory flow is the maximum

airflow rate during forced expiration. The

patient can use peak flow measurements to

check airway obstruction at home. The margin

of error in these measurement is 10–20%. The

European Respiratory Society recommends

taking the highest of the first three technically

good expirations.191 This technique is not

suitable for measuring the degree of

obstruction in COPD patients.

7. Provides information about the severity of the

disorder and the patient’s disease stage.

8. Provides information about load-bearing

capacity and about the disorders that have

developed because of adaptation to pulmonary

obstruction.

9. When the thorax is in a position characteristic

of inspiration, the anteroposterior and lateral

diameters of the thorax are greater, the

epigastric angle is obtuse, the ribs and clavicle

are more horizontal, and the distance between

the cricoid and the manubrium sterni is

smaller.14

10. Provides information on the load-bearing

capacity and about the disorders that have

developed because of adaptation to pulmonary

obstruction. Respiration or respiratory

movement may adapt before changes in the

position and shape of the thorax are visible.

11. Testing movement provides information about

load-bearing capacity and muscle function

impairments in the pulmonary patient. PImax

should be measured to assess the strength of

the respiratory muscles. Normal values are

given in terms of centimeters of water

(cmH2O). by Rochester and Arora:192 for

women between the ages of 19–49 years, the

normal value is -91 cmH2O; for women

between the ages 50–69, -77 cmH2O; for

women aged 70 years and over, -66 cmH2O; for

men aged 19–49 years, -127 cmH2O; for men

aged 50–69, -112 cmH2O; and for men aged 70

years and over, -76 cmH2O. If PImax is lower

than 70% of normal, respiratory muscle

34


V-03/2003/US

strength is reduced. A handheld dynamometer

can be used to assess the strength of other

peripheral muscles.193 For normal values and

further information, refer to Chapter 7 of the

Dutch project report.189

12. Provides information on the patient’s level of

stamina.

13. The walking test is a reliable measure of

stamina. Although the 12-minute test has

somewhat higher sensitivity, reliability and

discriminatory power,194 the 6-minute test is

recommended by the steering group because it

is quicker and, therefore, more practical. The

‘shuttle’ walking test is another option. More

information is given in the Dutch project

report.189

14. Pulse oximeters provide a non-invasive means

of estimating blood oxygen saturation. The

pulse oximeter used should be accurate during

exercise and sensitive to changes in oxygen

saturation up to a level of at least 90%. The

Hewlett-Packard and the Biox II pulse

oximeters meet these standards.195

15. The Borg scale is preferred by the steering

group because it has higher reliability and

stability and because its results correlate better

with respiration.196 The Borg scale is also

simpler to use and easier to standardize. Visual

analogue scales are good alternatives.196

35


V-03/2003/US

Abbreviations and glossary of terms

CNSLD chronic non-specific lung disease

COPD chronic obstructive pulmonary disease

FEV1 forced expiratory volume in one second

PImax maximum inspiratory pressure at the mouth

TLco transfer coefficient, expressing the diffusion capacity of the lung per unit of lung

volume (also known as DLco and Kco)

activity execution of a task or action by an individual

disability difficulties an individual may have in executing activities. Activities can be limited

in type, duration and quality.

huffing forced exhalation with an open glottis

coughing forced exhalation with a closed glottis

disorder abnormality in a body structure, or loss of or abnormality in a physiological or

psychological function

incidence of CNSLD number of new CNSLD patients in a given period of time

incremental exercise test maximum exercise test carried out under the supervision of a pulmonary physician,

during which various parameters are measured

participation involvement in a life situation, in the context of disorders, activities, health

condition and environmental factors. Participation can be restricted in type,

duration and quality

prevalence of CNSLD number of CNSLD patients at a given point in time

36


V-03/2003/US

1 Hendriks HJM, Reitzma E, van Ettekoven H. Centrale

richtlijnen in de fysiotherapie. Ned Tijdschr Fysiother

1996;106:2-11.

2 Hendriks HJM, van Ettekoven H, Reitzma E, Verhoeven ALJ,

van der Wees PhJ. Methode voor de centrale

richtlijnontwikkeling in implementatie in de fysiotherapie.

1998, Amersfoort, KNGF/NPi/CBO.

3 Bekkering GE, Hendriks HJM, Chadwick-Straver RVM,

Gosselink R, Jongmans M, Paterson WJ, van der Schans CP,

Verhoef-de Wijk MCE, Decramer M. Richtlijn voor het

fysiotherapeutisch handelen bij patiënten met chronisch

obstructieve longaandoeningen. Achtergronden en evaluatie

van de richtlijn COPD. 1998, Amersfoort, NPi.

4 Hendriks HJM, van Ettekoven H, van der Wees PhJ.

Eindverslag van het project Centrale richtlijnen in de

fysiotherapie (Deel 1). Achtergronden en evaluatie van het

project. 1998, Amersfoort, KNGF/NPi/CBO.

5 Hendriks HJM, Bekkering GE, van Ettekoven H Bransma JW,

van der Wees PhJ, de Bie RA. Development and

implementaion of national practice guidelines: A prospect

for continuous quality improvement in physiotherapy.

Introduction to the method of guideline development.

Physiotherapy 2000;86:535-547.

6 Bekkering GE, Hendriks HJM. Toelichting op de KNGF-

richtlijn COPD. Ned Tijdschr Fysiother 1998;108(5).

7 Deskundigheidbevorderingspakket KNGF-richtlijn COPD.

Fysiopraxis 1998.supplement

8 Hendriks HJM, van Ettekoven H, Bekkering GE, Verhoeven

ALJ. Implementatie van KNGF-richtlijnen. Fysiopraxis

2000;9:9-13.

9 Orie NGM, Sluiter HJ, de Vries K, Tammeling GJ, Witkop J.

The host factor in bronchitis. In: Orie NGM, Sluiter HJ,

editors. Bronchitis. Assen, the Netherlands: Royal van

Gorcum; 1961:43-59.

10 Sluiter HJ, Koeter GH, de Monchy JG, Postma DS, de Vries K,

Orie NG. The Dutch hypothesis (chronic non-specific lung

disease). revisited. Eur Respir J 1991;4:479-89.

11 Vermeire PA, Pride NB. A ‘splitting’ look at chronic

nonspecific lung disease (CNS-LD): common features but

diverse pathogenesis. Eur Respir J 1991;4:490-6.

12 Burrows B, Bloom JW, Traver GA, Cline MG. The course and

prognosis of different forms of chronic airways obstruction

in a sample from the general population. N Engl J Med

1987;317:1309-14.

13 Van Schayck CP. Het einde van de term CARA in zicht? [Is

the end of the term CNSLD in sight?] Ned Tijdschr

Geneeskd 1994;138:1405-8.

14 Gosselink HAAM, Cox N, Decramer M, Folgering HTM.

Fysiotherapie bij CARA. [Physical Therapy for CNSLD.] 3rd

ed. Utrecht, the Netherlands: Bunge; 1992.

15 American Thoracic Society. Standards for the diagnosis and

care of patients with chronic obstructive pulmonary disease.

ATS statement. Am J Respir Crit Care Med 1995;152:S77-

S120.

16 Siafakas NM, Vermeire P, Pride NB, Pooletti P, Gibson J,

Howard P et al. Optimal assessment and management of

chronic obstructive pulmonary disease (COPD). Eur Respir J

1995;8:1398-420.

17 American Thoracic Society. Lung function testing: selection

of reference values and interpretative strategies. Am Rev

Respir Dis 1991;144:1202.

18 Guyatt GH, Thompson PJ, Berman LB, Sullivan MJ,

Townsend M, Jones NL et al. How should we measure

function in patients with chronic heart and lung disease? J

Chronic Dis 1985;38:517-24.

19 McSweeny AJ, Grant I, Heaton RK, Adams KM, Timms RM.

Life quality of patients with chronic obstructive pulmonary

disease. Arch Intern Med 1982;142:473-8.

20 Okubadejo AA, Jones PW, Wedzicha JA. Quality of life in

patients with chronic obstructive pulmonary disease and

severe hypoxaemia. Thorax 1996;51:44-7.

21 Wijkstra PJ, ten Vergert EM, van de Mark TW, Postma DS,

van Altena R, Kraan J, Koeter GH. Relation of lung function,

maximal inspiratory pressure, dyspnoea, and quality of life

with exercise capacity in patients with chronic obstructive

pulmonary disease. Thorax 1994;49:468-72.

22 Williams SJ, Bury MR. Impairment, disability and handicap

in chronic respiratory illness. Soc Sci Med 1989;29:609-16.

23 American Thoracic Society. Standards for the diagnosis and

care of patients with chronic obstructive pulmonary disease

(COPD). and asthma. Am Rev Respir Dis 1987;136:225-44.

24 Kaptein AA, Dekker FW, Dekhuijzen PNR, Wagenaar JPM,

Janssen PJ. Patienten met chronische luchtwegobstructie.

Scores op NPV en scl-90 en hun relaties met functionele

capaciteit en belemmeringen in dagelijkse activiteiten.

[Patients with chronic airway obstruction. Scores on NPV

and scl-90 and their relationships to functional capacity and

limitations on activities of daily life.] Gezond Samenlev

1986;7:10-9.

25 Van de Lende R, Huygen C, Jansen-Koster EJ, Knijpstra S,

Peset R, Quanjer PH et al. Epidemiologisch onderzoek naar

het verband tussen luchtverontreiniging en het voorkomen

van luchtwegaandoeningen. [Epidemiological studies on the

relationship between air pollution and development of

respiratory disorders.] Ned Tijdschr Geneeskd 1975;119:577-

84.

26 Beaty TH, Menkes HA, Cohen BH, Newill CA. Risk factors

associated with longitudinal change in pulmonary function.

Am Rev Respir Dis 1984;129:660-7.

27 Knudson RJ, Knudson DE, Kaltenborn WT, Bloom JW.

Subclinical effects of cigarette smoking. A five-year follow-

up of physiologic comparisons of healthy middle-aged

smokers and nonsmokers. Chest 1989;95:512-8.

28 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-

49.

29 Higgins MW, Keller JB. Trends in COPD morbidity and

mortality in Tecumseh, Michigan. Am Rev Respir Dis

1989;140:S42-8.

30 Kauffmann F, Drouet D, Lellouch J, Brille D. Twelve years

spirometric changes among Paris area workers. Int J

Epidemiol 1979;8:201-12.

31 Heederik D, Pouwels H, Kromhout H, Kromhout D. Chronic

non-specific lung disease and occupational exposures

estimated by means of a job exposure matrix: the Zutphen

Study. Int J Epidemiol 1989;18:382-9.

32 Buist SA. Smoking and other risk factors. In: Murray JF,

37


V-03/2003/US

References

Nadel JA, editors. Textbook of respiratory medicine. 2nd ed.

Philadelphia: WB Saunders; 1994;1259-87.

33 Anthonisen NR, Wright EC, Hodgkin JE, IPPB Trial Group.

Prognosis in chronic obstructive pulmonary disease. Am Rev

Respir Dis 1986;133:14-20.

34 Prescott E, Lange P, Vestbo J. Chronic mucus hypersecretion

in COPD and death from pulmonary infection. Eur Respir J

1995;8:1333-8.

35 Wilson DO, Rogers RM, Wright EC, Anthonisen NR. Body

weight in chronic obstructive pulmonary disease. The

National Institutes of Health Positive-Pressure Breathing

Trial. Am Rev Respir Dis 1989;139:1435-8.

36 Postma DS, Burema J, Gimeno F, May JF, Smit JM, Steenhuis

EJ et al. Prognosis in severe chronic obstructive pulmonary

disease. Am Rev Respir Dis 1979;119:357-67.

37 Van de Lende R, Jansen-Koster EJ, Knijpstra S, Meinesz AF,

Wever AMJ, Orie NGM. Prevalentie van CARA in

Vlagtwedde en Vlaardingen (Computerdiagnose versus

artsendiagnose). [Prevalence of CNSLD in Vlagtwedde and

Vlaardingen (Computer diagnosis versus physician

diagnosis).] Ned Tijdschr Geneeskd 1975;119:1988-98.

38 Scenariocommissie Chronische Ziekten. Chronische ziekten

in het jaar 2005. Deel 2. Scenario’s over CARA 1990-2005.

[Scenario Commission on Chronic Diseases. Chronic

diseases in the year 2005. Part 2. Scenarios with CNSLD

1990-2005.] Houten/Antwerpen, the Netherlands/Belgium:

Bohn Stafleu van Loghum; 1990.

39 Van Molken MPMH, van Doorslaer EKA, Rutten FFH. CARA

in cijfers. Verslag van een pilotstudie. [CNSLD in figures.

Report on a pilot study.] 1989.

40 Gosselink HAAM, Wagenaar RC, van Keimpema A,

Chadwick-Straver RVM. Het effect van een

reactiveringsprogramma bij patiënten met CARA. [The effect

of a reactivation program among CNSLD patients.] Ned

Tijdschr Fysiother 1990;100:193-9.

41 Strijbos JH, Postma DS, van Altena R, Gimeno F, Koeter GH.

A comparison between an outpatient hospital-based

pulmonary rehabilitation program and a home-care

pulmonary rehabilitation program in patients with COPD. A

follow-up of 18 months. Chest 1996;109:366-72.

42 Wijkstra PJ, van de Mark TW, Kraan J, van Altena R, Koeter

GH, Postma DS. Long-term effects of home rehabilitation on

physical performance in chronic obstructive pulmonary

disease. Am J Respir Crit Care Med 1996;153:1234-41.

43 Van Valk RWA, Dekker J, Boschman M. Basisgegevens

extramurale fysiotherapie 1989-1992. [Basic data on

extramural physical Therapy 1989-1992.] 1995.

44 Uunk W, Dekker J, Groenewegen P. Verwijzingen van

huisartsen naar fysiotherapeuten: morbiditeits-specifieke

verwijspercentages. [Referrals by primary care physicians to

physiotherapists: morbidity-specific referral percentages.]

1991.

45 Cambach W, Chadwick-Straver RVM, Wagenaar RC, van

Keimpema A, Kemper HCG, Rijswijk H. Feasibility of a

pulmonary rehabilitation program in community-based

physiotherapy practices. J Rehab Sci 1994;7:104-12.

46 Wasserman K, Sue DY, Casaburi R, Moricca RB. Selection

criteria for exercise training in pulmonary rehabilitation. Eur

Respir J Suppl 1989;7:604s-10s.

47 Hendriks HJM, Wagner C, Dekker J, Brandsma JW. Evaluatie

van het ‘consultatief fysiotherapeutisch onderzoek’ (CFO).

in de eerstelijn. [Evaluation of the “consultative

physiotherapeutic examination” (CPE) in first-line care.]

1994.

48 Hoeksma BH, Keur M, Schreij HG. Tijdsbestedingsonderzoek

klinische fysiotherapie. [Time-allocation study of clinical

physiotherapy.] Enschede, the Netherlands: Hoeksma,

Homans and Menting; 1991.

49 Stubbing DG, Mathur PN, Roberts RS, Campbell EJ. Some

physical signs in patients with chronic airflow obstruction.


50 Richardson PS, Peatfield AC. The control of airway mucus

secretion. Eur J Respir Dis Suppl 1987;153:43-51.

51 Goodman RM, Yergin BM, Landa JF, Golinvaux MH, Sackner

MA. Relationship of smoking history and pulmonary

function tests to tracheal mucous velocity in non-smokers,

young smokers, ex-smokers, and patients with chronic

bronchitis. Am Rev Respir Dis 1978;117:205-14.

52 Van de Schans CP, van de Mark TW, Rubin BK, Postma DS,

Koeter GH. Chest physical therapy: mucus mobilizing

techniques. In: Bach JR, editor. Pulmonary rehabilitation.

The obstructive and paralytic conditions. Philadelphia:

Hanley and Belfus Inc; 1996;229-46.

53 Clarke SW, Jones JG, Oliver DR. Resistance to two-phase gas-

liquid flow in airways. J Appl Physiol 1970;29:464-71.

54 Mullen JB, Wright JL, Wiggs BR, Pare PD, Hogg JC. Structure

of central airways in current smokers and ex-smokers with

and without mucus hypersecretion: relationship to lung

function. Thorax 1987;42:843-8.

55 Mossberg B, Camner P, Afzelius BA. The immotile-cilia

syndrome compared to other obstructive lung diseases: a

clue to their pathogenesis. Eur J Respir Dis Suppl

1983;127:129-36.

56 Vestbo J, Prescott E, Lange P. The Copenhagen City Heart

Study Group. Association of chronic mucus hypersecretion

with FEV1 decline and chronic obstructive pulmonary

disease morbidity. Am J Respir Crit Care Med

1996;153:1530-5.

57 Folgering H, van Herwaarden C. Exercise limitations in

patients with pulmonary diseases. Int J Sports Med

1994;15:107-11.

58 Dekhuijzen PNR, Folgering HTM, van Herwaarden CLA.

Target-flow inspiratory muscle training during pulmonary

rehabilitation in patients with COPD. Chest 1991;99:128-33.

59 Bye PT, Esau SA, Levy RD et al. Ventilatory muscle function

during exercise in air and oxygen in patients with chronic

airflow limitation. Am Rev Respir Dis 1985;132:236-40.

60 Juan G, Calverley P, Talamo C, Roussos C. Effect of carbon

dioxide on diaphragmatic function in human beings. N Engl

J Med 1984;310:874-9.

61 McParland C, Krishnan B, Wang Y, Gallagher CG.

Inspiratory muscle weakness and dyspnea in chronic heart

failure. Am Rev Respir Dis 1992;146:467-72.

62 Donahoe M, Rogers RM, Wilson DO, Pennock BE. Oxygen

consumption of the respiratory muscles in normal and

malnourished patients with COPD. Am Rev Respir Dis

1989;140:385-91.

63 Decramer M, Lacquet LM, Fagard R, Rogiers P.

Corticosteroids contribute to muscle weakness in chronic

airflow obstruction. Am J Respir Crit Care Med 1994;

150:11-6.

64 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

38


V-03/2003/US

1989;140:1544-8.

65 Morrison NJ, Richardson J, Dunn L, Pardy RL. Respiratory

muscle performance in normal and elderly subjects and

patients with COPD. Chest 1989;95:90-4.

66 Cohen C, Zagelbaum G, Gross D, Roussos C, Macklem PT.

Clinical manifestations of inspiratory muscle fatigue. Am J

Med 1982;73:308-16.

67 Jones NJ, Jones G, Edwards RHT. Exercise tolerance in

chronic airway obstruction. Am Rev Respir Dis

1971;103:477-91.

68 Davidson AC, Leach R. George RJD, Geddes DM.

Supplemental oxygen and exercise ability in chronic

obstructive airways disease. Thorax 1988;43:965.

69 Light RW, Mahutte CK, Stansbury DW, Fischer CE, Brown

SE. Relationship between improvement in exercise

performance with supplemental oxygen and hypoxic

ventilatory drive in patients with chronic airflow

obstruction. Chest 1989;95:751-6.

70 Stein DA, Bradley BL, Miller WC. Mechanisms of oxygen

effects on exercise in patients with chronic obstructive

pulmonary disease. Chest 1982;81:6-10.

71 Killian KJ, Leblanc P, Martin DH, Summers E, Jones NL,

Campbell EJM. Exercise capacity and ventilatory, circulatory,

and symptom limitation in patients with chronic airflow

limitation. Am Rev Respir Dis 1992;146:935-40.

72 Maltais F, Simard AA, Simard C, Jobin J, Desgagnés P,

Leblanc P. Oxidative capacity of the skeletal muscle and

lactic acid kinetics during exercise in normal subjects and in

patients with COPD. Am J Respir Crit Care Med

1996;153:288-93.

73 Gosselink R, Troosters T, Decramer M. Peripheral muscle

weakness contributes to exercise limitation in COPD. Am J

Respir Crit Care Med 1996;153:976-80.

74 Minotti JR, Christoph I, Oka R, Weiner MW, Wells L, Massie

BM. Impaired skeletal muscle function in patients with

congestive heart failure. Relationship to systematic exercise

performance. J Clin Invest 1991;88:2077-82.

75 Schols AMWJ. Nutritional depletion and physical

impairment in patients with chronic obstructive pulmonary

disease. Implications for therapy. 1991.

76 Guz A. Respiratory sensations in man. Br Med Bull

1977;33:175-7.

77 Campbell EJM, Howell JBL. The sensation of breathlessness.

Br Med Bull 1963;19:36-40.

78 Burns BH, Howell JBL. Disproportionately severe

breathlessness in chronic bronchitis. Quart J Med

1969;151:277-94.

79 Mueller RE, Petty TL, Filley GF. Ventilation and arterial

blood gas changes induced by pursed-lips breathing. J Appl

Physiol 1970;28:784-9.

80 Celli BR, Rassulo J, Make BJ. Dyssynchronous breathing

during arm but not leg exercise in patients with chronic

airflow obstruction. N Engl J Med 1986;314:1485-90.

81 Geijer RMM, van Schayck CP, van Weel C, Sachs APE, van de

Zwan AAC, Bottema BJAM et al. NHG-Standaard COPD:

Behandeling. [NHG Guideline COPD: Treatment.] Huisarts

Wet 1997;40:430-42.

82 Engelen MPKJ, Schols AMWJ, Baken WC, Wesseling GJ,

Wouters EFM. Nutritional depletion in relation to

respiratory and peripheral skeletal muscle function in

outpatients with COPD. Eur Respir J 1994;7:1793-7.

83 Arora NS, Rochester DF. Effect of body weight and

muscularity on human diaphragm muscle mass, thickness

and area. J Appl Physiol 1982;52:64-70.

84 Schols AMWJ, Soeters PB, Dingemans AMC, Mostert R,

Frantzen PJ, Wouters EFM. Prevalence and characteristics of

nutritional depletion in patients with stable COPD eligible

for pulmonary rehabilitation. Am Rev Respir Dis

1993;147:1151-6.

85 Wilson DO, Rogers RM, Sanders MH, Pennock BE, Reilly JJ.

Nutritional intervention in malnourished patients with

emphysema. Am Rev Respir Dis 1986;134:672-7.

86 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;146:1511-7.

87 Brouwer T, Nonhof-Boiten JC, Uilreef-Tobi FC. Diagnostiek

in de fysiotherapie. Proces en denkwijze. [Diagnostics in

physical therapy. Process and approach.] Utrecht, the

Netherlands: Wetenschappelijke uitgeverij Bunge; 1995.

88 Van Ravensberg CD, Oostendorp RAB, Heerkens YF.

Diagnostiek, basis voor behandelplan en evaluatie.

[Diagnostics, a foundation for the treatment plan and

evaluation.] In: Vaes P, Aufdenkampe G, de Dekker JB, van

Ham I, Smits-Engelsman B, editors. Jaarboek fysiotherapie

kinesitherapie 1997. Houten/Diegem, the Netherlands:

Bohn Stafleu Van Loghum; 1997:302-25.

89 Oostendorp RAB, van Ravensberg CD, Wams HWA,

Heerkens YF, Hendriks HJM. Fysiotherapie; wat omvat het?

[Physical Therapy: What does it involve?] Bijblijven

1996;12:5-17, 39.

90 Kleijnen J, Knipschild P. Niacin and vitamin B6 in mental

functioning: a review of controlled trials in humans. Biol

Psychiatry 1991;29:931.

91 Kleijnen J, de Crean AJM, van Everdingen J, Krol L. Placebo

effect in double-blind clinical trials: a review of interactions

with medications. Lancet 1994;344:1347-9.

92 Pocock SJ. Clinical trials: a practical approach. Chisester, UK:

Wiley; 1983.

93 Meinert CL. Clinical trials: design, conduct and analysis.

New York: Oxford University Press; 1986.

94 Chalmers TC, Smith H, Blackburn B, Silverman B, Schroeder

B, Reitman D et al. A method for assessing the quality of a

randomized control trial. Control Clin Trials 1981;2:31-49.

95 Leith DE. Cough. Phys Ther 1968;48:439-47.

96 Langlands J. The dynamics of cough in health and in

chronic bronchitis. Thorax 1967;22:88-96.

97 Tammeling GJ, Quanjer PH. Contouren van de ademhaling

I. [Contours of breathing I.] 2nd ed. Leusden, the

Netherlands: Nederlands Astma Fonds; 1980.

98 Oldenburg FA, Dolovich MB, Montgomery JM, Newhouse

MT. Effects of postural drainage, exercise and cough on

mucus clearance in chronic bronchitis. Am Rev Respir Dis

1979;120:739-45.

99 Rossman CM, Waldes R, Sampson D, Newhouse MT. Effect

of chest physiotherapy on the removal of mucus in patients

with cystic fibrosis. Am Rev Respir Dis 1982;126:131-5.

100 Van de Schans CP, Piers DA, Beekhuis H, Koeter GH, van de

Mark TW, Postma DS. Effect of forced expirations on mucus

clearance in patients with chronic airflow obstruction; effect

of lung recoil pressure. Thorax 1990;45:623-7.

101 Van Hengstum M, Festen J, Beurskens C, Hankel M,

Beekman F, Corstens F. Effect of positive expiratory pressure

mask physiotherapy (PEP) versus forced expiration

39


V-03/2003/US

technique (FET/PD) on regional lung clearance in chronic

bronchitis. Eur Respir J 1991;4:651-4.

102 Olséni L, Midgren B, Hornblad Y, Wollmer P. Chest

physiotherapy in chronic obstructive pulmonary disease:

forced expiratory technique combined with either postural

drainage or positive expiratory pressure breathing. Respir

Med 1994;88:435-40.

103 Mortensen J, Falk M, Groth S, Jensen C. The effects of

postural drainage and positive expiratory pressure

physiotherapy on tracheobronchial clearance in cystic

fibrosis. Chest 1991;100:1350-7.

104 Van Hengstum M, Festen J, Beurskens C, Hankel M, van de

Broek W, Buijs W et al. The effect of positive expiratory

pressure versus forced expiration technique on

tracheobronchial clearance in chronic bronchitis. Scand J

Gastroenterol Suppl 1988;143:114-8.

105 Falk M, Kelstrup M, Andersen JB, Kinoshita T, Falk P,

Stovring S et al. Improving the ketchup bottle method with

positive expiratory pressure, PEP, in cystic fibrosis. Eur J

Respir Dis 1984;65:423-32.

106 Blake J. On the movement of mucus in the lung. J Biomech

1975;8:179-90.

107 Webber BA, Pryor JA. Physiotherapy skills: techniques and

adjuncts. In: Webber BA, Pryor JA, editors. Physiotherapy for

respiratory and cardiac problems. London, UK: Churchill

Livingstone; 1993:113-71.

108 Lannefors L, Wollmer P. Mucus clearance with three chest

physiotherapy regimes in cystic fibrosis: a comparison

between postural drainage, PEP and physical exercise. Eur

Respir J 1995;5:748-53.

109 Hofmeyr JL, Webber BA, Hodson ME. Evaluation of positive

expiratory pressure as an adjunct to chest physiotherapy in

the treatment of cystic fibrosis. Thorax 1986;41:951-4.

110 Wolff RK, Dolovich MB, Obminski G, Newhouse MT. Effects

of exercise and eucapnic hyperventilation on bronchial

clearance in man. J Appl Physiol 1977;43:46-50.

111 King M, Philips DM, Gross D, Vartian V, Chang HK, Zidulka

A. Enhanced tracheal mucus clearance with high frequency

chest wall compression. Am Rev Respir Dis 1983;128:511-5.

112 Pham QT, Peslin R, Puchelle E, Salmon D, Caraux G, Benis

AM. Respiratory function and the rheological status of

bronchial secretions collected by spontaneous expectoration

and after physiotherapy. Bull Eur Physiopath Resp

1973;9:293-311.

113 Hansen LG, Warwick WJ, Hansen KL. Mucus transport

mechanisms in relation to the effect of high-frequency chest

compression (HFCC) on mucus clearance. Pediatr Pulmonol

1994;17:113-8.

114 Thomas J, DeHueck A, Kleiner M, Newton J, Crowe J, Mahler

S. To vibrate or not to vibrate: usefulness of the mechanical

vibrator for clearing bronchial secretions. Physiother Can

1995;47:120-5.

115 Radford R, Barutt J, Billingsley JG, Hill W, Lawson H, Willich

W. A rational basis for percussion-augmented mucociliary

clearance. Respir Care 1982;27:556-63.

116 Wollmer P, Ursing K, Midgren B, Eriksson L. Inefficiency of

chest percussion in the physical therapy of chronic

bronchitis. Eur J Respir Dis 1985;66:233-9.

117 Pavia D. A preliminary study of the effect of a vibrating pad

on bronchial clearance. Am Rev Respir Dis 1976;113:92-6.

118 Groth S, Stafanger G, Dirksen H, Andersen JB, Falk M,

Kelstrup M. Positive expiratory pressure (PEP-mask)

physiotherapy improves ventilation and reduces volume of

trapped gas in cystic fibrosis. Bull Eur Physiopathol Respir

1985;21:339-43.

119 Menkes HA, Traystman RJ. Collateral ventilation. Am Rev

Respir Dis 1977;116:287-309.

120 Peters RM. Pulmonary physiologic studies of the

perioperative period. Chest 1979;76:576-84.

121 Van de Schans CP, van de Mark TW, de Vries G, Piers DA,

Beekhuis H, Dankert-Roelse JE et al. Effect of positive

expiratory pressure breathing in patients with cystic fibrosis.

Thorax 1991;46:252-6.

122 Williams MT. Chest physiotherapy and cystic fibrosis. Why

is the most effective form of treatment still unclear? Chest

1994;106:1872-82.

123 Konstan MW, Stern RC, Doershuk CF. Efficacy of the Flutter

device for airway mucus clearance in patients with cystic

fibrosis. J Pediatr 1994;124:689-93.

124 Pryor JA, Webber BA, Hodson ME, Warner JO. The flutter

VRP1 as an adjunct to chest physiotherapy in cystic fibrosis.

Respir Med 1994;88:677-81.

125 Schöni MH. Autogenic drainage: a modern approach to

physiotherapy in cystic fibrosis. J R Soc Med 1989;82:32-7.

126 Miller S, Hall DO, Clayton CB, Nelson R. Chest

physiotherapy in cystic fibrosis: a comparative study of

autogenic drainage and the active cycle of breathing

techniques with postural drainage. Thorax 1995;50:165-9.

127 Wijkstra PJ, van de Mark TW, Kraan J, Altena R van, Koeter

GH, Postma DS. Effects of home rehabilitation on physical

performance in patients with chronic obstructive

pulmonary disease (COPD). Eur Respir J 1996;9:104-10.

128 Berry MJ, Adair NE, Sevensky KS, Quinby A, Lever HM.

Inspiratory muscle training and whole body reconditioning

in chronic obstructive pulmonary disease. Am J Respir Crit

Care Med 1996;153:1812-6.

129 Strijbos JH, Koeter GH, Postma DS, van Altena R.

Reactivering van patiënten met chronische

luchtwegobstructie. [Reactivation of patients with chronic

airway obstruction.] Ned Tijdschr Fysiother 1989;99:302-7.

130 Weiner P, Azgad Y, Ganam R. Inspiratory muscle training

combined with general exercise reconditioning in patients

with COPD. Chest 1992;102:1351-6.

131 Goldstein RS, Gort EH, Stubbing D, Avendado MA, Guyatt

GH. Randomised controlled trial of respiratory

rehabilitation. Lancet 1994;344:1394-7.

132 Simpson K, Killian KJ, McCartney N, Stubbing DG, Jones

NL. Randomised controlled trial of weightlifting exercise in

patients with chronic airflow limitation. Thorax 1992;

47:70-5.

133 Cambach W, Chadwick-Straver RVM, Wagenaar RC, van

Keimpema ARJ, Kemper HCG. The effects of a community-

based pulmonary rehabilitation programme on exercise

tolerance and quality of life: a randomized controlled trial.

Eur Respir J 1997;10:104-13.

134 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;122:823-32.

135 Busch AJ, McClements JD. Effects of a supervised home

exercise program on patients with severe chronic obstructive

pulmonary disease. Phys Ther 1988;68:469-74.

136 Reid WD, Warren CPW. Ventilatory muscle strength and

endurance training in elderly subjects and patients with

40


V-03/2003/US

chronic airflow limitation. Physiother Canada 1984;

36:305-11.

137 Reardon J, Awad E, Normandin E, Vale F, Clark B, ZuWallack

RL. The effect of comprehensive outpatient pulmonary

rehabilitation on dyspnea. Chest 1994;105:1046- 52.

138 Wijkstra PJ, van Altena R, Kraan J, Otten V, Postma DS,

Koeter GH. Quality of life in patients with chronic

obstructive pulmonary disease improves after rehabilitation

at home. Eur Respir J 1994;7:269-73.

139 Lacasse Y, Wong E, Guyatt GH, King D, Cook DJ, Goldstein

RS. Meta-analysis of respiratory rehabilitation in chronic

obstructive pulmonary disease. Lancet 1996;348:1115-9.

140 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;97:1077-82.

141 Ries AL, Ellis B, Hawkins RW. Upper extremity exercise

training in chronic obstructive pulmonary disease. Chest

1988;93:688-92.

142 Ries AL, Archibald CJ. Endurance exercise training at

maximal targets in patients with chronic obstructive

pulmonary disease. J Cardiopulm Rehabil 1987;7:594-601.

143 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.

144 Maltais F, Leblanc P, Jobin J, Bérubé C, Bruneau J, Carrier L

et al. Intensity of training and physiologic adaptation in

patients with chronic obstructive pulmonary disease. Am J


145 Belman MJ, Shadmehr R. Targeted resistive ventilatory

muscle training in chronic pulmonary disease. J Appl

Physiol 1988;65:2726-35.

146 Goldstein R, de Rosie J, Long S, Dolmage T, Avendano MA.

Applicability of a threshold loading device for inspiratory

muscle testing and training in patients with COPD. Chest

1989;96:564-71.

147 Levine S, Weiser P, Gillen J. Evaluation of a ventilatory

muscle endurance training programme in the rehabilitation

of patients with chronic obstructive pulmonary disease. Am

Rev Respir Dis 1986;133:400-6.

148 Ries AL, Moser KM. Comparison of isocapnic

hyperventilation and walking exercise training at home in

pulmonary rehabilitation. Chest 1986;90:285-9.

149 Gigliotti F, Spinelli A, Duranti R, Gorini M, Goti P, Scano G.

Four-week negative pressure ventilation improves

respiratory function in severe hypercapnic COPD patients.

Chest 1994;105:87-94.

150 Patessio A, Rampulla C, Fracchia C, Joli F, Majani U, de

Marchi A et al. Relationship between the perception of

breathlessness and inspiratory resistive loading: report on a

clinical trial. Eur Respir J Suppl 1989;7:587s-91s.

151 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;138:689-96.

152 Preusser BA, Winningham ML, Clanton TL. High- vs low-

intensity inspiratory muscle interval training in patients

with COPD. Chest 1994;106:110-7.

153 Heijdra YF, Dekhuijzen PNR, van Herwaarden CLA,

Folgering HTM. Nocturnal saturation improves with target-

flow inspiratory muscle training in patients with COPD. Am

J Respir Crit Care Med 1996;153:260-5.

154 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;111:117-24.

155 Lisboa C, Villafranca C, Leiva A, Cruz E, Pertuze J, Borzone

G. Inspiratory muscle training in chronic airflow limitation:

effect on exercise performance. Eur Respir J 1997;10:537-42.

156 Wanke T, Formanek D, Lahrmann H, Brath H, Wild M,

Wagner C et al. The effects of combined inspiratory muscle

and cycle ergometer training on exercise performance in

patients with COPD. Eur Respir J 1994;7:2205-11.

157 Donner CF, Howard P. Pulmonary rehabilitation in chronic

obstructive pulmonary disease (COPD) with

recommendations for its use. Eur Respir J 1992;5:266-75.

158 Belman MJ, Warren CB, Nathan SD, Chon KH. Ventilatory

load characteristics during ventilatory muscle training. Am J


159 Belman MJ, Thomas SG, Lewis MI. Resistive breathing

training in patients with chronic obstructive pulmonary

disease. Chest 1986;90:662-9.

160 Gosselink R, Wagenaar RC, Decramer M. Reliability of a

commercially available threshold loading device in healthy

subjects and in patients with chronic obstructive pulmonary

disease. Thorax 1996;51:601-5.

161 Younes M. Determinants of thoracic excursions during

exercise. In: Whipp BJ, Wasserman K, editors. Exercise

pulmonary physiology and pathophysiology. vol 52. New

York: Marcel Dekker; 1991.

162 Ninane V, Rypens F, Yernault JC, de Troyer A. Abdominal

muscle use during breathing in patients with chronic airflow

obstruction. Am Rev Respir Dis 1992;146:16-21.

163 Reybrouck T, Wertelaers A, Bertrand P, Demedts M.

Myofeedback training of the respiratory muscles in patients

with chronic obstructive pulmonary disease. J Cardiopulm

Rehabil 1987;7:18-22.

164 Sergysels R, Willeput R, Lenders D, Vachaudez JP,

Schandevyl W, Hennebert A. Low-frequency breathing at

rest and during exercise in severe chronic obstructive

bronchitis. Thorax 1979;34:536-9.

165 Sharp JT, Druz WS, Moisan T, Foster J, Machnach W.

Postural relief of dyspnea in severe chronic obstructive

pulmonary disease. Am Rev Respir Dis 1980;122:201-11.

166 Druz WS, Sharp JT. Electrical and mechanical activity of the

diaphragm accompanying body position in severe chronic

obstructive pulmonary disease. Am Rev Respir Dis

1982;125:275-80.

167 O’Neill S, McCarthy DS. Postural relief of dyspnea in severe

chronic airflow limitation: relationship to respiratory muscle

strength. Thorax 1983;38:595-600.

168 Tiep BL, Burns M, Kao D, Madison R, Herrera J. Pursed-lips

breathing training using ear oximetry. Chest 1986;

90:218-21.

169 Thoman RL, Stoker GL, Ross JC. The efficacy of pursed-lips

breathing in patients with chronic obstructive pulmonary

disease. Am Rev Respir Dis 1966;93:100-6.

170 Gosselink RAAM, Wagenaar RC, Sargeant AJ, Rijswijk H,

Decramer MLA. Diaphragmatic breathing reduces efficiency

of breathing in chronic obstructive pulmonary disease. Am J


171 Sinclair DJM, Ingram CG. Controlled trial of supervised

exercise training in chronic bronchitis. BMJ 1980;1:519-21.

172 Cockcroft AE, Saunders MJ, Berry G. Randomised controlled

41


V-03/2003/US

trial of rehabilitation in chronic respiratory disability.

Thorax 1981;36:200-3.

173 Rosser R, Guz A. Psychological approaches to breathlessness

and its treatment. J Psychosom Res 1981;25:439-47.

174 Haas F, Salazar-Schicchi J, Axen K. Desensitization to

dyspnea in chronic obstructive pulmonary disease. In:

Casaburi R, Petti TL, editors. Principles and practice of

pulmonary rehabilitation. Philadelphia: WB Saunders; 1993.

175. Thornby MA, Haas F, Axen K. Effect of distractive auditory

stimuli on exercise tolerance in patients with COPD. Chest

1995;107:1213.

176 Kanters HW. Effectiviteit van patiëntenvoorlichting. Een

literatuuronderzoek. [Effectiveness of patient education. A

literature review.] Utrecht, the Netherlands: Landelijk

Centrum Dienstverlening; 1986.

177 Van Burgt M, Verhulst F. Doen en blijven doen.

Patiëntenvoorlichting in de paramedische praktijk. [Patient

education in paramedical practice.] Houten/Diegem, the

Netherlands: Bohn Stafleu Van Loghum; 1996.

178 Hoenen JAJH, Tielen LM, Willink AE. Patiëntenvoorlichting

stap voor stap: suggesties voor de huisarts voor de aanpak

van patiëntenvoorlichting in het consult. [Patient education

step by step: suggestions for the primary care physician in

approaching patient education during consultation.]

Uitgeverij voor gezondheidsbevordering Stichting O&O;

1988.

179 Knibbe NE, Wams HWA. Met patiëntenvoorlichting

methodisch werken aan therapietrouw. [Using patient

education to work methodically on therapeutic compliance.]

Ned Tijdschr Fysiother 1994;maart:44-51.

180 Dekkers F. Patiëntenvoorlichting: de onmacht en de pijn.

[Patient education: the powerlessness and the pain.] Baarn,

the Netherlands: Ambo; 1981.

181 Van Broek AHS. Patient education and chronic obstructive

pulmonary disease. 1995.

182 Sluijs EM. Patient education in physical therapy. 1991.

183 KNGF. Richtlijnen voor de fysiotherapeutische

verslaglegging. [Guidelines for physiotherapeutic report-

writing.] Amersfoort, the Netherlands: KNGF; 1993.

184 Cox NJM. Effects of a pulmonary rehabilitation programme

in patients with obstructive lung disease. Amsterdam, the

Netherlands: Thesis Publishers; 1990.

185 Guyatt GH, Berman LB, Townsend M, Pugsley SO, Chambers

LW. A measure of quality of life for clinical trials in chronic

lung disease. Thorax 1987;42:773-8.

186 Wijkstra PJ, ten Vergert EM, van Altena R, Otten V, Postma

DS, Kraan J et al. Reliability and validity of the chronic

respiratory questionnaire (CRQ). Thorax 1994;49:465-7.

187 Jones PW, Quirck FH, Baveystock CM. The St George’s

Respiratory Questionnaire. Respir Med 1991;85(suppl B):

25-31.

188 Jones PW, Quirck FH, Baveystock CM, Littlejohns P. A self-

complete measure of health status for chronic airflow

limitation. The St George’s Respiratory Questionnaire. Am

Rev Respir Dis 1992;145:1321-7.

189 Bekkering GE, Hendriks HJM, Chadwick-Straver RVM,

Gosselink R, Jongmans M, Paterson WJ et al. Richtlijn voor

het fysiotherapeutisch handelen bij patiënten met

chronische obstructieve longaandoeningen. Achtergronden

en evaluatie van de richtlijn COPD. [Guidelines for

physiotherapeutic management of patients with chronic

obstructive pulmonary disease. Background and evaluation

of the COPD guidelines.] Amersfoort, the Netherlands: NPi;

1998.

190 Werkgroep “Voorlichting aan CARA-patiënten”.

Voorlichting aan CARA-patiënten. Praktijk, theorie,

aanbevelingen. [Steering group “Information for CNSLD

patients.” Information for CNSLD patients. Practice, theory,

advice.] Utrecht, the Netherlands: Landelijk centrum GVO;

1988.

191 Quanjer PH, Tammeling GJ, Cotes JE, Pedersen OF, Peslin R,

Yernault JC. Lung volumes and forced ventilatory flows. Eur

Respir J 1993;6:5-40.

192 Rochester D, Arora NS. Respiratory muscle failure. Med Clin

North Am 1983;67:573-98.

193 Mathiowetz V. Reliability and validity of grip and pinch

strength measurements. Crit Rehab Phys Rehab Med

1991;2:201-12.

194 Garrett H, Vathenen S, Hill RA, Ebden P, Britton JR,

Tattersfield AE. A comparison of six- and twelve-minute

walk distance with 100-metre walk times in subjects with

chronic bronchitis. Thorax 1986;41:245.

195 Ries AL, Farrow JT, Clausen JL. Accuracy of two ear

oximeters at rest and during exercise in pulmonary patients.


196 Wilson RC, Jones PW. A comparison of the visual analogue

scale and modified Borg scale for the measurement of

dyspnoea during exercise. Clin Sci 1989;76:277-82.

42


V-03/2003/US

clinical practice guidelines for physical therapy in ... · on the basis of history-taking,...

Documents