Physiotherapy Practice Guidelines for COPD

PTCOC

March 2000

ii

Working Group Members Derek Chan, GH Galen Chan, HHH Charles Cheung, TMH Byran Chung, TPH David Yu, KH Annie Wu, ANNH Alice Chiu, QMH

1

I. Goals of Physiotherapy Practice Guidelines for COPD The goal of developing the physiotherapy practice guidelines for COPD is to provide evidence-based supports to the physiotherapy practice in COPD management within the Hospital Authority. It is an exercise of literature search and evaluation on related physiotherapy practices. Due to various constraints, the guidelines do not cover all, but some common physiotherapy assessments and treatment interventions used and studied in the field. Currently, there are several evidence-based clinical practice guidelines available providing generic disease management of COPD conditions (ATS, 1995; BTS, 1997; ERS, 1996). Although these documents are not physiotherapy specific, they form the backbone of the overall management model in this guideline. There are several reviews on pulmonary rehabilitation (Lacasse et al, 1996; ACCP/AACVPR, 1997; Cambach W et al, 1999; ATS, 1999) which constitute the base of this guideline on that particular subject. There are relatively few review on physiotherapy practice, but some recent metaanalysis focused on physiotherapy interventions on COPD (Jones & Rowe, 1999; Crockett AJ et al, 1999) are also included in this guidelines. Besides, other non-COPD specific evidence-based physiotherapy techniques guidelines, and COPD related primary studies are also cited and used in this guidelines, so as to compliment the discussion details of a particular practice. II. Epidemiology and Defintions of COPD A. Epidemiology of COPD There were total 10651 COPD patients admitted to the public hospitals throughout the territory in the year 1997,(HAHO, 1997) and they occupied over 20000 bed days. In average, each diagnosed patient admitted 2.31 times and their unplanned readmission rate was as high as 40.76%, which was the highest among all other disease groups. Unlike other chronic diseases utilized mostly the rehabilitation hospitals, over 50 % of the total COPD admissions were to acute hospitals. The data shown the huge demands of COPD patients on hospital services. B. COPD Definitions COPD is often used as a general term describing chronic lung disease, and its differentiation from other common chest conditions e.g. chronic bronchitis, emphysema and adult asthma is often confusing. Clarification of the terms is important, and the definitions used in the guideline are listed: Chronic obstructive pulmonary disease (COPD) is a chronic, slowly progressive disorder characterized by airflow obstruction (reduced FEV1 and FEV1/VC ratio) that does not change markedly over several months (BTS, 1997). The impairment of lung function is largely fixed but is partially reversible. The causes of airflow obstruction may due to chronic bronchitis or emphysema, or both.

2

Chronic bronchitis is defined as the presence of chronic productive cough for 3 months in each of two successive years in a patient in whom other causes of chronic cough have been excluded (ATS 1995). Emphysema is defined as abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis. (ATS 1995) Adult asthma is characterized by inflammation with participation of complex cellular and chemical mediators (ATS 1995), and the condition is reversible. Absolute clinical differentiation of severe COPD from chronic severe asthma is difficult since some degree of improvement in FEV1(reversibility)in COPD can often be produced by bronchodilator therapy(BTS, 1997). B. COPD Staging of Disease Severity of Symptoms COPD conditions are clinically classified into 3 stages: mild, moderate and severe, according to the patients' severity of symptoms (ERS 1995, BTS 1997). The stages are described as following (BTS, 1997): Mild stage : In patients with mild COPD there are few or no symptoms. A history of morning cough, recurrent respiratory infections, or shortness of breath on vigorous exertion or manual labour may happen. Moderate stage: Moderate COPD can present with a wide range of respiratory symptoms although there are few clinical signs. There is no single typical pattern but possibilities include combinations of some or all of the following:

- cough and sputum production, especially if the sputum becomes discoloured; - breathlessness(±wheeze) on moderate exertion such as physical work climbing hills; - acute worsening of symptoms associated with an infective exacerbation

Severe stage: Patients with severe COPD are usually troubled by progressively disabling breathlessness or with complications (such as the development of oedema) or with an acute exacerbation with or without respiratory failure. Cough and wheeze are almost invariably present but are poor predictors of severity. Spirometry findings Objective measurements of airways obstruction by FEV1 over predicted value is widely used as the physiological and practical indices for COPD severity classification. (ATS 1995, ERS 1995, BTS 1997) Table 1 illustrates COPD classifications according to FEV1 predicted values used by major medical societies. The classifications are similar, but with different reference points for management and treatment.

3

Table 1: Classification of severity of COPD based on FEV1 % of predicted value British Thoracic Society European Respiratory Society American Thoracic society Severity Mild Moderate Severe

FEV1 % pred 60-79 40-59 <40

Severity Mild Moderate Severe

FEV1 % pred ≥70 50-69 <50

Stage I II III

FEV1 % pred ≥50 35-49 <35

Functional Status Therapists may use patients' functional capacity as a reference for treatment interventions. Table 2 illustrate a commonly used functional classifications for COPD patients.(ATS, 1981) Class Functional capacity Signs and Symptoms A Full No dyspnoea on level walking

Dyspnoea on climbing 2 flight of stairs Insignificant COPD symptoms No restrictions imposed on the patient by his disease

B Slightly diminished No dyspnoea on level walking Dyspnoea on climbing 1 fight of stairs Mild COPD symptoms Slight restrictions with respect to strenuous activities and stress

C Significantly diminished Dyspnoea on walking 1.5 level city blocks at own pace Dyspnoea on some of the ADL Moderate COPD symptoms Considerable restrictions with respect to strenuous activities and stress; prolonged walking and standing are contraindicated, as well as lifting objects greater than 5 lbs

D Minimal remaining Dyspnoea on walking 0.5 level city block at own pace Dyspnoea on most minimal stair climbing Dyspnoea on most of the ADL Marked COPD symptoms Severe activity and environmental restriction, limiting patient to sedentary activities and the less demanding aspects of self-care

E No remaining Dyspnoea at rest Unable to carry out any of the ADL Severe COPD symptoms Maximal restrictions: patient is confined to wheelchair or bed; is complelely dependent on others, and can tolerate no environmental and emotional stress

4

III. Management of COPD A. COPD Management Model Early multidisplinary intervention is recommended for treating COPD patients (ATS 1995, BTS 1997). Once the diagnosis of COPD is established, the patient should be educated about the disease and encouraged to actively participate in therapy (ATS 1995). For stable COPD, the management varies according to the stages of the diseases. The COPD Escalator summaries the therapies recommended, and its appropriate time of introduction according to the stage of disease (BTS 1997) (Fig 1). Pulmonary rehabilitation is a generally recommended as a major component in COPD management (ATS 1995, BTS 1997, ERS 1995) The COPD Escalator

Fig 1 The COPD Escalator: Summary of the principal components of a management plan for COPD (modified from BTS Guideline for COPD)

Ass

essm

ent f

or

LTO

T A

mbu

lato

ry o

xyge

n

Influ

enza

vac

cina

tion

Pulm

onar

y re

habi

litat

ion

Mor

e fr

eque

nt/c

ombi

natio

n br

onch

odila

tors

St

eroi

d re

veer

sibi

lity

trial

: in

hale

d st

eroi

ds if

+ve

Occ

asio

nal b

ronc

hodi

lato

r as r

equi

red

Ant

ibio

tics f

or a

cute

infe

ctio

ns

Smok

ing

cess

atio

n

Healthy population

Smoker's cough Little or no dyspnoea No abnormal signs

Dyspnoea on exertion Cough and sputum Some abnormal signs

Dyspnoea on mild exertion Hyperinflation and cyanosis

Death

Increasing investigation and treatment

FEV

1 as

% p

redi

cted

20

80

100

0

Symptoms

5

Acute exacerbation of COPD present as a worsening of previous stable situation. Mild cases can be treated in the community or at Emergency Unit, and many others will be admitted as inpatients (BTS 1997). As in-patient, drugs as bronchodilators, antibiotics and corticosteroids are crucial in controlling the acute symptoms. Stepwise drug therapy with rapid response is recommended for uses (ATS 1995). Oxygen therapy is introduced and adjusted to correct hypoxemia, and aims SaO2>90% (BTS 1997). Physiotherapy is commonly referred to treat patients' chest related impairments. Prior discharge, a comprehensive discharge plan for individual patient is recommended, so as to facilitate the long term caring of the disease(ATS 1995, BTS 1997). B. Objectives of Physiotherapy

1. Physiotherapy in unstable exacerbations

- to control symptoms - to treat related chest problems e.g. sputum retention - to minimize disability - to recruit and plan for pulmonary rehabilitation

2. Physiotherapy in stable COPD - to improve physical fitness and cardiopulmonary function - to improve functional status and minimize disability - to enhance life quality and social roles - to educate and coach for activity modifications

C. Physiotherapy Assessment Physiotherapy assessments of COPD patients include measures of impairments, disabilities and handicaps. There is a wide spectrum of assessment tools available to evaluate the patients' conditions. Choosing appropriate tools is important and the choice depends on the treatment objectives and patients' disease status. 1. Chest Assessment Chest assessment is widely used among physiotherapists as a means to evaluate the extent and severity of respiratory impairments of COPD patients. It is extensively maneuvered for COPD patients at all stages of the disease, whether stable or exacerbated. Chest assessment contains package of assessment items (PTCOC, 1994), which are not tailored for COPD, but general lists for chest conditions evaluations. During exacerbation, chest assessment is important for physiotherapist to plan appropriate interventions. Interventions like postural drainage therapy is not a routine treatment, but for indicated cases(AARC, 1992). For stable patients or patients under rehabilitation programs, chest assessment is still useful for cases having chest problems, likes(Singh SJ 1997) :

6

- recurrent chest infections - difficulties with chest clearance - inappropriate shortness of breath after exercise - abnormal breathing patterns - inappropriate inhaler technique

2. Assessment for pulmonary rehabilitation Since pulmonary rehabilitation is a team program, the assessment for COPD patients should be a collaborated process. Physiotherapist involves in the assessment process, but the practice and extent of involvement varies among different program designs. American Thoracic Society stated a comprehensive assessment of the rehabilitation candidate is necessary for the development of an appropriate, individualized plan of care, and generally, the assessment should include (ATS 1999):

1. Clinical history 2. Physical examination 3. Review of pertinent records e.g. spirometry 4. Educational assessment 5. Incremental exercise testing 6. Measurements of respiratory muscle strength 7. Measurements of peripheral muscle strength 8. Assessments of activities of daily living 9. Assessments of health status 10. Assessments of cognitive function, emotional and mood state 11. Assessments of nutritional status/body composition

3. HRQOL assessment Disease specific and generic instruments are available to measure health-related QOL of candidates of pulmonary rehabilitation program. The Outcomes Committee of the American Association of Cardiovascular and Pulmonary Rehabilitation recommended the uses of Chronic Respiratory Questionnaries(CRQ) and St. George's Respiratory Questionnaries (SGRQ)(Pashlow et al, 1995). Although generic HRQOL instruments e.g. Short-form-36 Health Survey (SF-36) may provide complementary information, they appear to be less responsive to therapeutic interventions(Donald, 1998).

The CRQ developed by Guyatt and colleagues is a 20-items questionnaries evaluating four dimensions of illness: dyspnea, fatigue, emotional function and mastery. Reliability and validity estimates for the CRQ had been reported (Guyatt, 1987).

The SGRQ is a self-administrated 76-items questionnaries measuring three domains: symptoms, activity and impact of disease on daily life. The "symptoms" category elicits information about cough, sputum, wheeze and dyspnea. The "activities" reflects the activity limitation imposed by the disease and the "impacts" reflect overall impact on daily life and well-being. The SGRQ has been translated into several languages and reliability and validity estimates have been reported(Jones, 1992).

7

4. Dyspnea Rating According to ATS official statement, dyspnea is a term used to characterize a subjective experience of breathing discomfort that consists of quantitatively distinct sensations that vary in intensity (ATS, 1999). Often dyspnea is out of portion to the degree of impairment of lung function and arterial blood gas analysis (Sweer & Zwillich, 1998), and is derived from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses (ATS, 1999). Pathophysiologic factors of dyspnoea is appended for reference (Appendix III). In assessing patient's severity or evaluating treatment outcomes, both exertional and overall dyspnea should be measured. Exertional dyspnea is usually rated during exercise testing, while overall dyspnea is commonly assessed through its impact on daily activities. Dyspnea during exercise is usually measured with a category scale as Borg scale of perceived exertion or a visual analog scale(VAS).A modified version Borg 10-point scale with verbal expression of severity (Borg, 1976) was widely used in pulmonary rehabilitation programs. A Chinese version is attached for reference (Appendix IV). The Visual Analogue Scale (VAS) consists of a line, usually 100 mm in length, placed either horizontally or vertically on a page (Grit, 1989), with anchor to indicate extremes of a sensation. Scoring is accomplished by measuring the distance from the bottom of the scale to the level indicated by the subject. The day-to-day overall dyspnea can be measured by different instruments as the Medical Research Coucil(MRC) dyspnea questionaire, the University of California San Diego Sortness of Breath Questionnaire(UCSD-SOBQ), the dyspnea component of the Chronic Respiratory Disease Questionnaire, the Baseline and Transitional Dyspnea Indexes(BDI and TDI), and the Pulmonary Functional Status and Dyspnea Questionaire(PFSDQ) and its modified version(PFSDQ-M) (ATS, 1999). One of the most commonly used dyspnea instument is BDI. It is used to measure breathlessness at a single point in time and is administered during a brief interview. BDI includes measurement of functional impairment (the degree to which activities of daily living are impaired) and magnitude of effort (the overall effort exerted to perform activities), in addition to magnitude of task (Mahler et al, 1984). Most recently, the University of California at San Diego Shortness of Breath Questionnaire (USCDQ) was developed. The UCSDQ is a 24-item questionnaire measuring dyspnea during the past week (Belman et al, 1996). In the modified version, patients are asked about the frequency of dyspnea when performing 21 different activities inquire about activity limitations due to shortness of breath, fear of harm from overexertion, and fear of shortness of breath (Eakin et al, 1995). 5. Walking Tests

Timed walking tests namely 6 Minutes Walk Test, 12 Minutes Walk Test and Shuttle Walk Test are used to assess patient's functional ability of walking. These tests are simple and convenient to perform. The tests correlate with peak exercise performance on graded exercise tests and self

8

reported data on functional test (ATS 1999). Standardization of test procedures is crucial to have reliable findings (ATS 1999). The progressive 10-m Shuttle Walk Test differ from ordinary timed walk tests in two aspects. It is an incremental exercise test in nature, which rather measure exercise capacity than endurance. Since the external sets the pace, self-pacing is eliminated. The Shuttle Walk Test is reproducible, correlate with maximum oxygen consumption during incremental treadmill exercise and highly responsive to therapeutic intervention (ATS 1999).

D. Physiotherapy Interventions 1. Bronchopulmonary Hygiene 2. Breathing retraining 3. Pulmonary Rehabilitation

3.1 Exercise Reconditioning 3.2 Education

4. Alternative treatment modalities 1. Bronchopulmonary Hygiene A metaanalysis on the effectiveness of bronchopulmonary hygiene physiotherapy techniques was conducted by Jones AP and Rowe BH in 1998(Jones & Rowe, 1998). The patient samples include not just COPD, but also bronchiectasis patients.7 RCTs are included in the review, and the results are summaried as following: 1. Demonstrable beneficial effects of bronchopulmonary hygiene physiotherapy techniques

BHPT have been confined to sputum production and radio-aerosol clearance only. 2. The impact of BHPT on lung function is not clearly established from studies includes in the

review. No study found a significant beneficial effect on pulmonary function or PaO2. 3. It is not possible from the trails reviewed to identify specific patients subgroups that might

benefit from BHPT. 4. Insufficient reporting in publications precludes any comments on the adverse effects or harm

associated with BHPT. 5. In view of the lack of functional improvement and sample sizes of the trials, the research on

BHPT is inconclusive. There is insufficient evidence to support or refute administration of BHPT to patients with acute and stable COPD, chronic bronchitis or bronchiectasis.

Due to the limited quantity and quality of the reviewed RCTs, the review left many unanswered questions. The review stated the research implications as: 1. there is a need to conduct RCTs of sufficient power that examine the effects of the various

forms of BHPT, both manual and mechanical 2. These trails should be conducted in clearly defined patient groups, with adequate controls,

randomization and blinding. In addition, such studies need to measure not only primary function. They also should measure symptoms, exercise performance, health status(quality of life), recovery time and relapse rate.

9

3. There also is a need to examine various BHPT regimens, rather than a single treatment. The review searched the related RCTs till July 1997, and the types of the BHPT included in the review: postural drainage, manual techniques, directed coughing and forced exhalation techniques(FET). 1.1 Coughing/Forced expiratory technique

There are evidence that both cough and FET can clear radioaerosol particles induced to lungs field (Bennett WD et al, 1981; Hasani A et al, 1991; Van der Schans 1990). Since the presence of severe obstructive airways and bronchospasm may hamper the effectiveness of directed cough(AARC, 1993), advantages of FET over cough had been suggested as less energy demand (Langlands J, 1967), and better mucus transport effect(van der Schans et al, 1990 ). Directed cough or FET can be readily used as an integral part other physiotherapy techniques as postural drainage (Olseni L et al, 1994). Indications of the coughing and FET was suggested (AARC, 1993):

- the need to aid in the removal of retained secretions from central airways - the presence of atelectasis - as prophylaxis against postoperative pulmonary complications - as a routine part of bronchial hygiene in patients with cystic fibrosis,

bronchiectasis, chronic bronchitis, necrotizing pulmonary infection, or spinal cord injury

- as an integral part of other bronchial hygiene therapies 1.2 Postural Drainage Therapy In AARC Clinical Practice Guideline on Postural Drainage Therapy (PDT), PDT is defined to include turning, postural drainage, percussion, vibration, and cough (AARC 1991). In actual clinical practice, physiotherapist should select appropriate techniques for treating indicated COPD patients. Although COPD is not the primary diagnosis that indicated for PDT, unlike cystic fibrosis, bronchiectasis and cavitating lung disease(AARC, 1991), PDT still pertains its roles in various chest problems and complications e.g. sputum retention. Earlier studies support PDT can effectively clear secretion, without altering the pulmonary parameters (Sutton et al, 1983; Newton & Stephenson, 1978; Bateman, 1979). Sutton et al (1983) reported that a 30 minutes period of PD alone doubled the sputum production and improved tracheobronchial clearance above control. Newton and Stephenson(1978) found that the PDT including PD, percussion, vibration and breathing exercise significantly improve both functional residual capacity and the airway conductance of acute patients with chronic bronchitis. Improvement in airway conductance attributed to an altered distribution of sputum in the larger airways. Bateman et al ((1979) showed that the PDT significantly increased clearance of sputum from central, intermediate and peripheral lungs regions. There is no evidence PDT causing harm to COPD patients. Buscaglia et al (1983) studied the oxygen saturation during PDT on acute patients with COPD, and showed that PDT did not appear to produce dangerous hypoxaemia

10

even on acutely ill patients with severe COPD. Other studies on PDT is complied in Appendix VI for reference. 2. Breathing Retraining Breathing Retraining for COPD patients may be started early during the inpatient admission period at excerabation, and continued throughout their rehabilitative and maintenance phases. There are many techniques used by physiotherapists for such purposes, some common names include breathing control, pursed-lip breathing, diaphragmatic breathing. The adjunct positioning and relaxation skills are also important to achieve good training results. 2.1 Breathing Control/Active Control Breathing Technique Breathing control at rest is defined as gentle breathing using the lower chest with relaxation of the upper chest and shoulders; it is performed at normal tidal volume, at a natural rate, and expiration should not be forced (Webber & Pryor, 1993). Slow and controlled breathing produced an increase in tidal volume and a reduction in the arterial partial pressure of carbon dioxide (PaCO2)(Mortley, 1963) . It is common that breathing control is taught and practiced during activities in pulmonary rehabilitation. Few researches had, however, been done on this technique and its usefulness during activities. Another commonly used breathing retraining technique for COPD is Active Control Breathing Technique ACBT (Miller et al, 1995; White et al, 1996). Its effectiveness reflected in some trials in treating cystic fibrosis, but with limited evidence in managing COPD conditions. 2.2 Diaphragmatic Breathing Diaphragmatic breathing is to consciously expand the abdominal wall during inspiratory diaphragm descent. In theory, this would increase the efficiency of the diaphragm while reducing the ineffective movement of upper chest wall and accessory muscle works. Despite the theory, studies had demonstrated that taught diaphragmatic breathing increased the sensation of dyspnoea and asynchrony of the chest wall, and reduced mechanical efficiency with COPD (Vitacca et al, 1998; Gosselink et al, 1995). In view of the results, the routine use of diaphragmatic breathing training in pulmonary rehabilitation is not recommended(ATS, 1999). 2.3 Pursed-lips breathing Pursed-lips breathing is a technique commonly adopted by some COPD patients, typically those with some degree of emphysema. The lips are pursed during expiration, creating some end-expiratory pressure and thus maintaining small-airway patency. This technique has been documented to reduce respiratory rate, and to increase tidal volume and oxygen saturation (Webber & Pryor, 1993; Mueller et al, 1970; Tiep et al, 1986). Despite these physiologic outcomes, the effectiveness of purse-lip breathing in reducing dyspnea in COPD is controversial, with some studies actually demonstrating an increase in breathlessness at rest and during exercise (ATS, 1999).

11

2.4 Positioning Physiotherapists used to teach or help patients to adopt a relaxed position to relief dyspnea during acute exacerbation of COPD. There are, however, limited studies on the efficacy of the practise, and research study is rarely found in 1990s. Positioning affect the efficiency of breathing mechanism. Most COPD patients prefers leaning forward position. Such position had the greatest Pimax and least work of breathing in comparing to other positions(O Neil & McCarthy, 1983), and effectively reduced the sensation of breathlessness (Sharp et al, 1980). For COPD patients, sitting is usually more comfortable than supine position, and the Pimax and Pemax is higher in sitting position (Heijdra e al, 1994). Activities cause greater respiratory demand to COPD than healthy subjects( Baarends et al, 1995), hence mastering of comfortable and less demanding positions may be an important teaching component in COPD management. 3. Pulmonary Rehabilitation Pulmonary rehabilitation programs are used to be delivered in either in-patient or out-patient models. Both delivery models of pulmonary rehabilitation showed promising result of patient's outcomes. Recently, there were researches to study the feasibility and effectiveness of home-based rehabilitation for COPD patients (Strijbos JH et al, 1996; Wiljkstra PJ et al, 1994, Bauldoff Gs et al, 1996). At present, there is no consensus on optimal practices of pulmonary rehabilitation (ATS, 1999). Questions on what are the essential components and cost-effectiveness of pulmonary rehabilitation had been raised and remained unanswered (ACCP/AACVPR, 1997). Pulmonary rehabilitation is a multidisplinary program, and physiotherapists share roles as one of the team member. Physiotherapists involve in education and some psychosocial interventions, but exercise therapy remains the distinct contribution in pulmonary rehabilitation. 3.1 Exercise Reconditioning 3.1.1 Training Principles Aims of Exercise reconditioning

- to improve muscle strength and endurance - to improve cardiopulmonary fitness - to minimize disabilities and maximize functional abilities - to enhance psychological wellbeing

Tolerance training Exercise tolerance training is often termed aerobic or endurance exercise training. Exercise tolerance improvement is not just based upon the overall exercise regimes prescribed to the patients, but also the synergy effects of all the elements in the rehabilitation program. In general pulmonary rehabilitation practice, walking with or without treadmill, and stationary cycling are

12

two common exercises prescribed for cardiopulmonary and tolerance training. The frequency and intensity of exercises prescribed vary among programs. Strength Training Peripheral muscle strength influence exercise performance of COPD patients, and its relation was shown in 6 minutes walking performance(Troosters T et al, 1996). The strength of Quadriceps contributes significantly to six minutes walking distance and maximal oxygen uptake (Hamilton N et al, 1995; Gosselink R et al, 1996). Relative few studies have evaluated the effectiveness of strength training in COPD patients. Despite of this, there is evidence that peripheral strengthening exercises not only can improve muscles functions (O'hara WJ et al, 1984; Simpson K et al, 1992; Clark CJ et al, 1996), but also can have positive effects on overall exercise performance (O'hara WJ et al, 1984; Clark CJ,1996)and quality of life(Simpson K et al,1992) as well. Training Intensity Use of heart rate as a descriptor of aerobic exercise intensity is widely applicable. In healthy subjects, aerobic training is usually targeted at 60 to 90% of the predicted maximal heart rate Recently, American Thoracic Society suggested higher training intensity of 60%-75% of maximal heart rate as an effective training zone for COPD patients(ATS, 1999). For those who cannot tolerate long period (20 to 30 minutes) of high intensity training, interval training with 2 to 3 minutes high intensity exercise and equal period of rest, may be an alternative(ATS, 1999). Beside heart rate, use of dyspnea ratings (Borg-scale either for dyspnea or leg fatigue) obtained from a maximal graded exercise test can also be reliably as a training target to produce specific exercise intensities in symptom-guided exercise training (Horowitz et al, 1996). American college of sports medicine considered the impairment level of different COPD patients and suggested 4 different approaches in exercise prescription (ACSM, 1995): 1. Exercise at 50% of Maximum Oxygen Uptake (VO2max or VO2peak): for patients with

moderate to severe COAD who are deconditioned, training at this threshold intensity for improvement of aerobic capacity should improve exercise performance.

2. Exercise at intensity above the anaerobic threshold (AT): for patients with mild COAD to reduce VE and lactate. Use heart rate as a monitor. (AT and VO2max should be obtained from Cardiopulmonary Exercise Test).

3. Exercise at a near-maximal intensity: for patients with moderate to severe COAD who can sustain ventilation at a high percentage of their maximal minute ventilatory volume. It is suggested that 95% of VO2peak for a few minutes can increase endurance.

4. Use ratings of dyspnea to define intensity: for patients with moderate to severe COAD who are limited by exertional dyspnea. Target dyspnea rating is 3 (moderate) for exercise training at an intensity of 50% VO2peak and 6 (between severe and very severe) for training at an intensity of 85% VO2peak

13

3.1.2 Lower extremity training In pulmonary rehabilitation, lower extremity training is often used as a major means for endurance and cardiopulmonary training for COPD patients. The training effects is well documented, and include improve peak oxygen consumption (Peak VO2) (Ries AL et al, 1995; Wijkstra PJ et al,1994) reduce minute ventilation (VE) (O'Donnell DE et al, 1995), improve timed walking distance (McGavin CR et al, 1977; Cockcroft AE et al, 1981; Lake FR, 1990; Alison JA, 1981; Goldstenin RS, 1994), improve maximum working capacity (Alison JA et al, 1981) and decrease dyspnea ratings (Reardon J et al, 1994; Ries AL et al, 1995; O'Donnell DE et al, 1995). ACCP/AACVPR recommendations (Appendix VII) The strength of evidence is graded A. COPD patients who undergo a program of lower extremity exercise training consistently improve measures of exercise tolerance without evidence of adverse outcome. A program of exercise training of the muscles of ambulation is recommended as part of pulmonary rehabilitation. Common lower extremities exercises include cycle ergometer training, treadmill walking, ground-based walking, or combined exercises. Studies showed that all exercises are effective in improving maximal work rate and endurance(ATS, 1999).Reviewed studies varied considerably in training design: durarion, frequency, and intensity(ACCP/AACVPR, 1997). Only a few studies describe their training regimen in great detail (Casaburi R et al, 1991; Maltais F et al, 1996). The optimal specific training regimens for patients with COPD still be defined(ACCP/AACVPR, 1997). 3.1.3 Upper extremity training Upper limbs endurance training is important to COPD patients for their daily activities, and it is common for COPD patients report limitations of ADL involving the upper extremities(Tangri & Woolf, 1973). Upper extremity training can improve exercise capacity of upper extremity (Ries AL et al, 1988), and decrease ventilatory demand for similar arm work (O'Tiara WJ et al, 1984). The effect of upper extremity training alone is less effective than lower extremity training in improving overall function.(Ries Al et al, 1988; Lake FR et al, 1990) The addition of upper extremity training to lower extremity training can significantly improve functional status when compared to either exercise alone(Lake FR et al, 1990) ACCP/AACVPR recommendations The strength of evidence is graded B. Strength and endurance of the upper extremities improve arm function in COPD patients. Arm exercises are safe, and should be included in rehabilitation programs for COPD patients. Patients can perform upper limbs exercises with arms supported or not. The supported arm exercise commonly prescribed is upper limb ergometer, while unsupported arm exercises by free weights, dowels and stretching elastic bands. Either training methods can effectively improve arm endurance(ATS, 1999), though it was suggested that unsupported arms exercises have better

14

functional outcomes(Martinez FJ et al, 1993). There is no standard way to train the arms, but ACCP/AACVPR had illustrated two forms of common upper extremity training (ACCP/AACVPR, 1997).Upper extremity ergometer training is achieved by having patients cycle at approximately 50 rpm. The load increases at 5-W intervals from zero until 20 to 30 min of exercise. The arms can also be trained by lifting weight up to shoulder level , the weights are increased as tolerated until 20 to 30 min of exercise . The patient's performance is monitored with arms fatigue and dyspnea . 3.1.4 Inspiratory Muscle Training IMT Inspiratory muscle function may be compromised in COPD, an impairment that may contribute to dyspnea, exercise limitation and hypercapnia (ATS, 1999). Inspiratory muscle training (IMT) is exercise specifically designed to build endurance and strength of the muscles powering the ventilatory pump, aimed to minimize patients' disabilities. ACCP/AACVPR recommendations The strength of evidence is graded B. The scientific evidence at present time does not support the routine use of IMT as an essential component of pulmonary rehabilitation. However, IMT may be considered in selected patients with COPD who have decrased respiratory muscle strength and breathlessness. Echo to the ACCP/AACVPR recommendations, after reviewing 7 mixed interventions, Lacasse concluded that the evidence of IMT confers any additional benefit to COPD pulmonary rehabilitation is equivocal (Lacasse et al, 1996). The recent metaanalysis of long term pulmonary effect on pulmonary rehabilitation also shared the same view (Cambach et al, 1999). Although the beneficial effects of IMT alone on disabilities and handicaps of COPD patients remained inconclusive (ATS 1999), there are clear evidence that IMT increase inspiratory muscle strength (Gosselink R, 1997), reducing dyspnea and improving exercise tolerance of COPD patients (Sonne et al, 1982; Falk et al, 1985; Goldstein et al, 1989; Reid & Dechman, 1995). There have been large variations in IMT program and training methods. Respiratory muscle strength is usually estimated by measuring maximal negative inspiratory pressure (Pimax), and the minimal load required to achieve a training effect is 30% of the Pimax (Smith et al, 1992) The 3 main types of IMT are sustained hyperpnea, resistive loading and threshold loading(Appendix VIII). Training systems for sustained hyperpnea are institutional and require monitoring, while the last 2 methods are convenient for patients self-practise and have been studied more extensively. 3.2 Psychosocial and Education Interventions Depression, anxiety and selected psychiatric symptoms are common in patients with COPD. There is a positive association of psychological distress with pulmonary impairment, poor body image, increased loneliness, reduced social support, dissatisfaction with social support and

15

negative self concept (Nicholas PK et al, 1992; Keele CG et al, 1993; Kersten L et al, 1990) .There is also documented impairment on tests of cognitive or neuropsychological functioning among COPD patients, indicating deficits in higher-level cognitive tasks such as attention, complex visual motor processes, abstraction ability and verbal tasks ( Incalzi Ra et al, 1993;Grant I et al, 1982; Fix AJ et al, 1982) Pulmonary rehabilitation programs usually include psychosocial or behavioral components in addition to exercise training. It can be in the forms of educational talks, patient support groups, or stress management groups (Emery CF et al, 1991;Ries AL et al, 1995).There are Multidisciplinary involvement in such service, and physiotherapy may share roles in such interventions. ACCP/AACVPR recommendations The strength of evidence is graded C. Evidence to date does not support the benefits of short-term psychosocial interventions as single therapeutic modalities, but long-term interventions may be beneficial. Although scientific evidence is lacking, expert opinion supports the inclusion of educational and psychosocial interventions as components of comprehensive pulmonary rehabilitation programs for COPD patients. Exercise training itself is also a means to improve COPD patients' psychological wellbeing. Benefits of exercises are both physiologic and psychological. Psychological benefits such as increase motivation, antidepressant effects of exercise, loss of fear of dyspnea, desensitization to dyspnea (Iiaas F et al, 1993), improve skill of performance (Paez PN et al, 1967; Pierce AK, 1964). 4. Alternative treatment modalities 4.1 Flutter Aiding expectoration is an important factor for patients suffering form bronchial hypersecretion. The Flutter valve was developed in Switzerland in the late 1980s as a hand-held mucus clearance device designed to combine PEP with airway oscillation Most of the evidence of effectiveness of Flutter was found in patients with cystic fibrosis(Konstan M et al, 1994; Ernst M et al, 1998). Weiner et al studied the effect of Flutter in COPD patients (n=20). After 3 months of treatment, lung function (FEV1 and FVC) as well as 12 minutes walk test were higher than those performing the placebo Flutter. Arterial blood gases, the maximum voluntary ventilation, and respiratory rate at rest were unchanged in both groups. (Weiner P et al, 1996). 4.2 Long Term Oxygen Therapy LTOT COPD patients usually develop progressive hypoxemia, which can rapidly lead to damaging cellular hypoxia. The administration of domiciliary long term oxygen therapy (LTOT) can be life preserving, and physiotherapist may share roles in the management. The Cochrane Group's

16

metaanalysis on 4 related RCTs concluded LTOT improves survival in a selected group of COPD patients with severe hypoxaemia(arterial PO2 is less than 8.0kPa), and it does not appear to improve survival in patients with moderate hypoaemia nor in COPD patients with nocturnal desaturation only( Crockett et al, 1999). Patients survival is one of the major outcome measures in evaluating LTOT effectiveness. Two of the four RCTs included in the review, NOTT and MRC, demonstrated a significant survival advantage for the selected COPD subjects receiving LTOT. In the NOTT study there was a significant improvement in mortality for hypoxaemic COPD patients after 24 months of treatment with continuous LTOT over nocturnal oxygen therapy group(NOTT, 1980). In the MRC study LTOT produced a small but significant overall improvement in survival in patients with chronic lung diseases(MRC, 1981). Beside survival, other outcome measures as HRQOL and physiological parameters also found in related studies, but was not included in the metaanalysis. According to American Thoracic Society (ATS) statement 1995, COPD patients whose disease is stable on a full medical regimen, with PaO2 < 55 mmHg (<7.3kPa or corresponding to an SaO2 < 88%), should receive long term oxygen therapy LTOT. A patients whose PaO2 is between 55 and 59 mmHg (SaO2 89%) and who exhibits signs of tissue hypoxia, such as cor pulmonale, erythrocytosis, edema from right heart failure, or impaired mental status, should receive LTOT (ATS, 1995). Concerning the exercise-induced breathlessness, portable oxygen therapy should be recommended only for patietns emonstrating a clear improvement of >50% in exercise tolerance or breathlessness on exercise (Leach et al, 1994). 4.3 Non-invasive Positive Pressure Ventilation Patients with acute exacerbation of COPD are prone to develop acute respiratory failure and is associated with high mortality. Some patients are treated with intubation and mechanical ventilation but this carries a high morbidity and may have difficulty in weaning off. These problems have led to the use of non-invasive positive pressure ventilation (NIPPV) (Doherty & Greenstone, 1998). NIPPV was first introduced in 1987(Ellis et al, 1987). The benefit of NIPPV over conventional treatment in selected exacerbated COPD patients with respiratory failure had been documented in some RCTs (Bott et al, 1993; Brochard et al, 1995; Kramer et al, 1995). The proven benefits includes improved arterial blood gas tensions, decreased breathlessness, reduced intubation needs, reduced mortality and length of hospital stay. A metaanalysis of NIPPV in exacerbations of respiratory failure due to COPD is developing by the Cochrane Group to evaluate its effectiveness.

17

4.4 Acupuncture Acupuncture has traditionally been used in asthma (a condition overlaps with COPD) treatment in China, and is increasingly applied in other countries. A recent Cochrane review stated there is inconclusive evidence that short term(1-12 weeks) acupuncture treatment has a significant effect on the course of asthma (Linde K et al, 1998), and there is an urgent need for quality research. Few trials specifically evaluated the side-effect and morbidity profile of acupuncture treatments, but the overall safety profile appears to be excellent (Linde K et al,1998). Despite of the controversial on acupuncture for asthma, its development worth our concern. At present, there is no review of acupuncture on COPD as the primary diagnosis. A RCT was conducted to compare two group COPD patients received acupunture and placebo acupunture respectively, the acupunture group had significant benefit in subjective breathlessness and six minutes walk scores. ( Jobst K et al, 1986)

18

References 1. ACCP/AACVPR Pulmonary rehabilitation guidelines panel (1997). Pulmonary rehabilitation:

Joint ACCP/ AACVPR Evidence-based guidelines. Chest 112 (5): 1363 – 1395. 2. Alison JA, Samilos R, Anderson SD (1981). Evaluation of Exercise Training in Patients with

Chronic Air Obstruction. Phys Ther 61(9): 1273-1277. 3. American college of sports medicine (1995). ACSM's Guidelines for Exercise Testing and

Prescription. 5th ed, Williams & Wilkins. 4. American Thoracic Society (1981). Executive Committee Statement. March 1981. 5. American Thoracic Society (1999). Pulmonary rehabilitation. Am J Respir Crit Care Med

159 : 1666-1682. 6. American Thoracic Society (1995). Standards for the diagnosis and care of patients with

chronic obstructive pulmonary disease. Am J Respir Crit Care Med 152: 77-120. 7. American Thorcic Society (1962). Chronic bronchitis, asthma, and pulmonary emphysema: a

statement by the committee on diagnostic standards for nontuberculous respiratory diseases. Am Rev Respir Dis 85:762-768.

8. Baarends EM, Schols AM, Slebos DJ, et al(1995). Metabolic and ventilatory response pattern to arm elevation in patients with COPD and healthy age-matched subjects. Eur Respir J 8(8): 1345-1351

9. Bateman JRM, Newman SP, Daunt KM, Pavia D, Clarke SW (1979). Regional lung clearance of excessive bronchial secretions during chest physiotherapy in patients with stable chronic airways obstruction. Lancet February:294-297.

10. Bateman JRM, Newman SP, Daunt KM, Sheahan NF, Pavia D, Clarke SW (1981): Is cough as effective as chest physiotherapy in the removal of excessive tracheobronchial secretions? Thorax 36:683-687.

11. Bauldoff Gs, Hoffman LA, Sciurba F, Zullo TG (1996). Home-based, upper-arm exercise training for patients with chronic obstructive pulmonary disease. Heart Lung 25 (4):288-294.

12. Belman MJ, Botnick WC, Shin JW (1996). Inhaled bronchodilator reduce dynamic hyperinflation and exercise capacity in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 153:967-975.

13. Bennett WD; Foster WM; Chapman WF(1990). Cough-enhanced mucus clearance in the normal lung. J Appl Physiol 69(5): 1670-1675

14. Borg G (1976). Simple rating methods for estimation of perceived exertion Wenner-Gren Center International Symposium Series 28:39-47.

15. Bott J, Carroll MP, Conway JH (1993). Randomized controlled trail of nasal ventilation in acute ventilatory failure due to chronic obstructive airways disease, Lancet 341:1555-1557.

16. British Thoracic Society (1997). BTS guidelines for the management of chronic obstructive pulmonary disease. Thorax 52(Suppl 5): 26-28.

17. Brochard L, Mancebo J, Wysocki M (1995). Non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease, N Engl J Med 333:817-822.

18. Buscaglia AJ and St. Marie MS (1983): Oxygen saturation during chest physiotherapy for acute exacerbation of severe chronic obstructive pulmonary disease. Respiratory Care 28:1009-1013.

19. Cambach W, Wagenaar RC, Koelman TW, Ton van Keimpema ARJ (1999). The long-term effects of pulmonary Rehabilitation in patients with asthma and chronic obstructive pulmonary disease : A research synthesis, Arch. Phys. Med. Rehabil. 80:103-111.

19

20. Casaburi R, Patessio A, Ioli F, Zanaboni S, Donner CF, Wasserman K(1991).. Reductions in exercise lactic acidosis and ventilation as a result of exercise training in patients with obstructive lung disease. Am Rev Respir Dis 143: 9-18.

21. Christensen EF, Nedergaard T, Dahl R (1990): Long-term treatment of chronic bronchitis with positive expiratory pressure mask and chest physiotherapy. Chest 97:645-650.

22. Clark CJ, Cochrane JE, ackay E.(1996). Low intensity peripheral muscle conditioning improves exercise tolerance and breathlessness in COPD. Eur Respir J 9: 2590-2596.

23. CockcroftAE, Saunders MJ, Berry G (1981). Randomised controlled trial of rehabilitation in chronic respiratory disability. Thorax 36: 200-203

24. Crockett AJ, Moss JR, Cranston JM, Alpers JH (1999). Domicilary oxygen in chronic obstructive pulmonary disease(Cochrane Review). In: The Cochrane Library, Issue 3, 1999. Oxford: Update Software.

25. Doherty MJ, Greenstone MA (1998), Survey of non-invasive ventilation (NIPPV) in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) in the UK, Thorax 53:863-866.

26. Eakin EG, Sassi-Dambron DE, Ries AL, Kaplan RM (1995). Reliability and validity of dyspnea measures in patients with obstructive lung disease Int. J. Behav. Med. 2:118-134.

27. Ellis ER, bye PTP, Brunderer JW, Sullivan CE (1987). Treatment of respiratory failure during sleep in patients with neuromuscular disease, Am Rev Respir Dis 135:148-152.

28. Emery CF, Leatherman NE, Burker EJ, et al (1991). Psychological outcomes of a pulmonary rehabilitation program. Chest 100:613-617.

29. Ernst M, Kieselmann RT, Reinhardt D, et al.(1998). Sputum rheology changes in cystic fibrosis lung disease following two different types of physiotherapy. Chest 114:171-177.

30. European Respiratory Society (1995).Optimal assessment and management of chronic obstructive pulmonary disease (COPD). The Eur Respir J 8:1398-1420.

31. Falk P, Eriksen A-M, Kolliker K, Andersen JB (1985). Relieving dyspnea with severe airflow limitation. Eur J Respir Dis 66: 181 – 186.

32. Fix AJ, Golden CJ, Daughton D, et al(1982). Neuropsychological deficits among patients with chronic obstructive pulmonary disease. Int J Neruosci16:99-105.

33. Gallon A (1991): Evaluation of chest percussion in the treatment of patients with copious sputum production. Respir Med 85:45-51.

34. Goldstein R, DeRosie J, Long S, Dolmage T, Avendano MA (1989). Applicability of a threshold loading device for inspiratory muscle testing and training in patients with COPD. Chest 96: 564 - 571.

35. Goldstenin RS, Gort EII, Stubbing D, et al(1994). Randomised controlled trial of respiratory rehablitation. Lancet 344: 1394-1397.

36. Gosselink RA, Wagenaar RC, Sargcant AJ, Rijswijk H et al (1995) Diaphragmatic breathing reduces efficiency of breathing in chronic obstructive pulmonary disease. Am. J. Respir. Crit. Care Med. 151:1136-1142.

37. Gosselink R, Troosters T, Decramer M(1996). Peripheral muscle weakness contributes to exercise limitation in COPD. Am J Respir Crit Care Med 153: 976-980.

38. Gosselink R, Troosters T, DecramerM 1997 Exercise training in COPD patients: the basic questions. Eur Respir J 10: 2884-2891.

39. Grant I, Heaton RK, McSweeny AJ, et al (1982). Neuropsychological findings among patients with chronic obstructive pulmonary disease. Arch Intern Med 142:1470-1476.

40. Grit AG (1989). Validation of a vertical visual analogue scale as a measure of clinical dyspnea Rehab. Nurs 14:313-325.

20

41. HAHO Statistics & Health Information Section (1997). Epidemilogical Report for Hong Kong Public Hospital Services.

42. Hamilton N, Killian KJ, Summers E, Jones NL(1995). Muscle strength, symptom intensity, and exercise capacity in patients with cardiorespiratory disorders. Am J Respir Crit Care Med 152: 2021-2031.

43. Hasani A, Pavia D, Agnew F et al (1991). The effect of unproductive coughing/FET on regional mucus movement in the human lungs. Respir Med. 85(suppl A):23-26.

44. Hasani A, Pavia D, Agnew JE, et al. Regional mucus transport following unproductive cough and forced expiration technique in patients with airway obstruction.

45. Heijdra YF, Dekhuijzen PN, van Herwaarden CL, et al(1994). Effects of body position, hyperinflation, and blood gas tensions on maximal respiratory pressures in patients with chronic obstructive pulmonary disease. Thorax 49:453-458

46. Horowitz MB, Littenberg B, Mahler DA (1996). Dyspnea ratings for prescribing exercise intensity in patients with COPD. Chest 109:1169-1175.

47. Iiaas F, Saiazar-Schicchi J, Axen K(1993). Desensitation to dyspnea in chronic obstructive pulmonary disease. In: Casaburi R, Petty TL, eds. Principles and practice of pulmonary rehabilitation. Philadelphia: WB Saunder: 241-251.

48. Incalzi RA, Gemma A Marra C et al (1993). Chronic obstructive pulmonary disease: an original model of cognitive decline. Am Rev Respir Des 148: 418-424.

49. Jones AP, Rowe BH 1998. Bronchopulmonary hygiene physical therapy in chronic obstructive pulmonary disease and bronchiectasis. The Cochrane Library. Issue 4

50. Keele Card G, Foxall MJ, Barron CR (1993). Loneliness, depression and social support of patients with COPD and their spouses. Public Health Nurs 10-245-51.

51. Kersten L (1990) Changes in self concept during pulmonary rehabilitation part I. Heart Lung 19:456-62.

52. Konstan M, Stern R, Doershuk C (1994). Efficacy of the Flutter device for airway mucus clearance in patients with cystic fibrosis. J of Pediatr 124:689-693.

53. Kramer N, Meyer TJ, Meharg J (1995). Randomized prospective trial of noninvasive positive pressure ventilation in acute respiratory failure, Am J Respir Crit Care Med 151:1799-1806.

54. Lacasse Y, Guyatt GH, Goldstein RS (1997). The components of a respiratory rehabilitation program: a systematic overview. Chest 111(4): 1077-1088

55. Lake FR, Henderson K, Briffa T, et al (1990).Upper-limb and lower-limb exercise training in patients with chronic airflow obstruction. Chest 97: 1077-1082.

56. Langenderfer B (1998): Alternatives to percussion and postural drainage. Journal of Cardiopulmonary Rehabilitation 18:283-289.

57. Langlands J (1967). The dynamics of cough in health and chronic bronchitis. Thorax 22:88-96.

58. Leach RM, Bateman NT (1994): Domiciliary oxygen therapy. British J of Hosp Medicine 51:47-54.

59. Linde K, Jobst K, Panton J (1998). Acupuncture for the treatment of asthma bronchiale (Cochrane Review). In: The Cochrane Library, Issue 4. Oxford: Update Software.

60. Mahler D, Weinberg CW, Feinstein A (1984). The measurement of dyspnea : contents, interobserver agreement and physiologic correlates of two new clinical indexes Chest 85:751-758.

61. Maltais F, Leblanc P, Simard C, et al.(1996). Skeletal muscle adaptation to endurance training in patients with chronic obstructive pulmonary disease. Am J.Respir Crit Care Med. 154: 442-447.

21

62. Martinez FJ, Vogel PD, Dupont DN, Stanopoulos I, Gray A, Beamis JF (1993). Supported arm exercise vs unsupported arm exercise in the rehabilitation of patients with severe chronic airflow obstruction. Chest 103 (5): 1397-1402.

63. May DB and Munt PW (1979): Physiologic effects of chest percussion and postural drainage in patients with stable chronic bronchitis. Chest 75:29-32.

64. Mazzocco MC, Owens GR, Kirilloff LH, Rogers RM (1985): Chest percussion and postural drainage in patients with bronchiectasis. Chest 88:360-363.

65. McGavin CR, Artvinli M, Naeo H (1978). Dyspnea, disability, and distance walked: comparison of estimates of exercise performance in respiratory disease BMJ 2:241-243.

66. McGavin CR, Gupta SP, Lioyd EL, et al(1977). Physical rehabilitation for the chronic bronchitis: results of a controlled trial of exercise in the home. Thorax 32: 307-311.

67. Medical Research council Working Party (1981). Long term domcilliary oxygen therapy in chronic hypoxic cor-pulmonale complicating chronic bronchitis and emphysema Lancet 1:681-686.

68. Miller S, Hall DO, Clayton CB, Nelson R (1995): Chest physiotherapy in cystic fibrosis: a comparative study of autogenic drainage and the active cycle of breathing techniques with postural drainage. Thorax 50:165-169.

69. Morgan M; Singh S (1997). Practical pulmonary rehabilitation. Chapman & Hall, London:23-43.

70. Mortensen J, Falk M, Groth S, Jensen C (1991): The effects of postural drainage and positive expiratory pressure physiotherapy on tracheobronchial clearance in cystic fibrosis. Chest 100:1350-1357.

71. Mueller RE, Petty TL and Filley (1970). GK Ventilation and arterial blood gas chances induced by pursed lips breathing. J. Appl. Physiol 28:784-789.

72. #Newton DAG and Stephenson (1978): Effect of physiotherapy on pulmonary function. Lancet :228-230.

73. Nicholas PK, Leuner JD(1992). Relationship between body image and chronic obstructive pulmonary disease. Appl Nurs Res 5:83-88.

74. Nocturnal Oxygen Therapy Trail Group (1980). Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trails Ann. Intern. Med. 93:391-398.

75. O Neill S; McCarthy DS(1983). Postural relief of dyspnoea in severe chronic airflow limitation: relationship to respiratory muscle strength. Thorax 38(8): 595-600.

76. O'Donnell DE, McGuire M, Samis L, et al (1995). The impact of exercise reconditioning on breathlessness in severe chronic airflow limitation. Am J Respir Crit Care Med 152:2005-13.

77. O'hara WJ, Lasachuk KE, Matheson PC, Renahan MC, Schlotter DG, Lilker ES(1984). Weight training and backpacking in chronic obstructive pulmonary disease. Respir Care 29: 1202-1210.

78. Olseni L, Midgren B, Hornblad Y et al (1994).Chest physiotherapy in chronic obstructive pulmonary disease: forced expiratory technique combined with either postural drainage or positive expiratory pressure breathing. Respir Med 88:435-440.

79. Paez PN, Phillipson EA, Mosangkay M, et al (1967). The physiologic basis of training patients with emphysema. Am Rev Respir Dis 95: 944-953.

80. Pierce AK, Taylar HF, Archer RK, et al (1964). Responses to exercise training in patients with emphysema. Arch Intern Med 113: 28-36.

81. Reardon J, Awad E, Normandin E, et al. (1994) The effect of comprehensive outpatient pulmonary rehabilitation on dyspnea. Chest 105: 1046-1052.

22

82. Ries AL, Ellis B, Hawkins RW(1988). Upper extremity exercise training in chronic obstructive pulmonary disease. Chest 93: 688-692.

83. Ries AL, Kaplan RM Limber TM, et al(1995). Effects of pulmonary rehabilitation on physiologic and psychosocial outcomes in patients with chronic obstructive pulmonary disease. Ann Intern Med 122:823-32

84. Rivington-Law BA, Epstein SW, Thompson GL, Corey PN (1984): Effect of chest wall vibrations on pulmonary function in chronic bronchitis. Chest 85:378-381.

85. Sharp JT, Drutz WS, Moisan T, et al(1980). Postural relief of dypsnea in severe chronic obstructive pulmonary disease. Am Rev Resp Dis 122:201-211.

86. Simpson K, Killian kj, McCartney N, Stubbing DG, Jones NL(1992). Randomised controlled trial of weightlifting exercise in patients with chronic airflow limitation. Thorax 47: 70-75.

87. Sonne LJ, Davis JA 1982. Increased exercise performance in patients with severe COPD following inspiratory resistive training. Chest 81: 436 – 439.

88. Stiller K, Geake T, Taylor J, Grant R, Hall B (1990): Acute lobar atelectasis: A comparison of two chest physiotherapy regimens. Chest 98:1336-1340.

89. Strijbos JH, Postma DS, van Altena R, et al (1996).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 109(2): 366-72.

90. Tangri S, Woolf CR.(1973) The breathing pattern in chronic obstructive lung disease during performance of some common daily activities. Chest 63: 126-127.

91. Tiep BL, Burns M, Kao D et al(1986). Pursed lips breathing training using ear oximetry. Chest 90:218-21.

92. Troosters T, Gosselink R, Rollier H, Decramer M (1996). Change in lower limb muscle strength contributes to altered six minutes walking distance in COPD. Eur Respir J 9: 144.

93. Van der Schans CP, Piers DA, Beekhuis H, et al (1990). Effect of forced expirations on mucus clearance in patients with chronic airflow obstruction: effect of lung recoil pressure. Thorax 45:623-627.

94. Van der Schans CP, Piers DA, Postma DS (1986): Effect of manual percussion on tracheobronchial clearance in patients with chronic airflow obstruction and excessive tracheobronchial secretion. Thorax 41:448-452.

95. Van-Hengstum M, Festen J, Beurskens C, Hankel M, van den Broek W, Buijs W, Corstens F (1988): The effect of positive expiratory pressure versus forced expiration technique on tracheobronchial clearance in chronic bronchitics. Scand J Gastroenterol: Suppl:114-118.

96. Vitacca M, Clini E, Bianchi L et al (1998) Acute effects of deep diaphragmatic breathing in COPD patients with chronic respiratory insufficiency. Eur Respir J 11:408-425.

97. Webber, BA. and Pryor JA (1993) Physiotherapy skills: techniques and adjuncts. In Physiotherapy for Respiratory and Cardiac Problems (eds B.A. Webber, and J.A. Pryor). Edinburg: Churchill Livingstone :113-171.

98. Weiner P, Zamir D, Waizman J, et al (1996). [Physiotherapy in chronic obstructive pulmonary disease: oscillatory breathing with flutter VRP1] Harefuah 131:14-7, 71(Abstract only).

99. White D, Stiller K, Wilson K (1996): The role of thoracic expansion exercises during the active cycle of breathing techniques. 13:155-162.

100. Wijkstra PJ, Van Altena R, Kraan J, et al(1994). Quality of life in patients with chronic obstructive pulmonary disease improves after rehabilitation at home. Eur Respir J 7 (2): 269-73.

23

101. Jobst KA, Chen JH, McPherson K, Arrowsmith J., Brown V., Efthimiou J., Fletcher HJ, Maciocia G., Mole P., Shifrin K., Lane DJ (1986). Controlled trial of acupuncture for disabling breathlessness. Lancet 2:1416-1419.

24

Appendix 1. Pathophysiological factors of Dyspnoea 2. Chinese version of Modified Borg Scale 3. Summery table of Postural Drainage Therapy studies 4. Grading of ACCP/AACVPR Practice Guidelines 5. Training methods of IMT 6. Standardization of 6 minutes walk test

25

Appendix I : Pathophysiological factors of dyspnoea Table illustrates the pathophysiologic factors in COPD that promotes breathlessness: Increased airways resistance Elevated minute ventilation due to inefficient gas exchange Hyperinflation resulting in Reduced ability of diaphragm to generate tension Reduced efficiency of diaphragm in generation of negative intrathoracic pressure Reduced outward recoil of chest wall Respiratory muscle weakness Respiratory muscle fatigue Recruitment of needed accessory respiratory muscles during arm exercise Posture Hypoxemia and hypercapnea Pulmonary hypertension

26

Appendix II: Chinese version of Modified Borg Scale 0 沒甚麼 0.5 非常, 非常輕微 (剛可感到) 1 非常輕微 2 輕微 (微量) 3 中量 4 稍為強烈 5 強烈 (沉重) 6 7 非常強烈 8 9 10 非常, 非常強烈 (接近頂點)

頂點 自我評估氣促表 (RPD). Borg Category Ratio Scale for Perceived Dyspnea From: Borg, G. Medicine and science in sports and Exercise, 1982

27 Appendix III: Table of some Postural Drainage Therapy Studies Investigators Patient Comparison Study Design Measurement Results Postural Drainage (PD) Olseni et al (1994) COPD PD+FET

PD+PEP RCT Mucus Clearance Both effective

Patients preferred to use PEP Newton & Stephenson (1978)

Chronic Bronchitis

Chest physio. PD vibration percussion Breathing ex.

RCT FEV1, VC, FRC, airways resistance & conductance, blood gases

symbol 221 \f "Symbol" \s 12⇑} FRC & airways conductance. Returned to baseline 40 min. after physio..

Bateman et al (1979) Stable COPD Chest physio. PD vibration percussion

RT cross-over Sputum clearance symbol 221 \f "Symbol" \s 12⇑} sputum clearance

van-Hengstum et al (1988) Chronic bronchitis

PEP+Br.+huffing+ cough

FET+PD+Br. Ex.

RT cross-over Sputum clearance PD + FET is more effective than PEP + FET

Buscaglia and St. Marie (1983)

COPD Positioning Clinical trial O2 saturation No production of dangerous hypoxemia.

May and Munt (1979) Chronic bronchitis

Percussion + PD Heat

Clinical trial Sputum production. Lung function. Blood gases.

symbol 221 \f "Symbol" \s 12⇑} sputum production. Others- no change.

Stiller et al (1990) Lobar atelectasis PD + vibration + bagging + suction

Bagging + suction

RT Resolution of atelectasis PD group symbol 174 \f "Symbol" \s 12→} symbol 221 \f "Symbol" \s 12⇑} the efficacy of the treatment regime.

Mazzocco et al (1985) Bronchiectasis PD + percussion RCT FVC, SpO2, FEV1, HR, PEF, sputum amount.

symbol 221 \f "Symbol" \s 12⇑} sputum production especially those large sputum producer.

Mortensen et al (1991) CF PD + FET PEP + FET

RCT cross-over Sputum clearance Similar effect in both groups.

28 Percussion & Vibration Newton & Stephenson (1978)

Chronic Bronchitis

Chest physio. PD vibration percussion Breathing ex.

RCT FEV1, VC, FRC, airways resistance & conductance, blood gases

symbol 221 \f "Symbol" \s 12⇑} FRC & airways conductance. Returned to baseline 40 min. after physio..

May and Munt (1979) Chronic bronchitis

Percussion + PD Heat

Clinical trial Sputum production. Lung function. Blood gases.

symbol 221 \f "Symbol" \s 12⇑} sputum production. Others- no change.

Bateman et al (1979) Stable COPD Chest physio. PD vibration percussion

RT cross-over Sputum clearance symbol 221 \f "Symbol" \s 12⇑} sputum clearance

Bateman et al (1981) PD + vibration + shaking + percussion.

Cough.

RCT cross-over Sputum clearance. Sputum yielded more during chest PT than during cough.

Buscaglia and Marie (1983) COPD Positioning Clinical trial O2 saturation No production of dangerous hypoxemia. Mazzocco et al (1985) Bronchiectasis PD + percussion RCT FVC, SpO2, FEV1, HR,

PEF, sputum amount. symbol 221 \f "Symbol" \s 12⇑} sputum production especially those large sputum producer.

Van der Schans (1991) CAO Percussion. PD + percussion + coughing +

breathing ex.. PD + coughing + breathing ex..

RCT cross-over Sputum clearance Percussion may be useful when patient is not able to cough and cannot assume the appropriate position for PD.

Gallon (1991) Bronchiectasis PD + deep breathing ex. (DBE) + FET

PD + DBE + FET + fast manual percussion

PD + DBE + FET + slow manual percussion

RCT cross-over Sputum clearance Both fast and slow manual percussion increase the sputum production.

Rivington-Law et al (1984) Chronic bronchitis

DBE DBE + vibration

RCT cross-over FRC - ERV RV

SpO2

Vibration does not decrease ERV in patient with chronic bronchitis but DBE does.

29

Appendix IV Grading of ACCP/AACVPR Practice Guidelines Grade Description A Scientific evidence provided by well-designed, well

conducted, controlled trials (randomized and nonrandomized) with statistically significant results

B Scientific evidence provided by observational studies or by controlled trials with less consistent results

C Expert opinion. Scientific evidence available did not present consistent results or controlled trails were lacking

Appendix V: Training methods of IMT Inspiratory resistive loading Patient inspires through a nonlinear resistive device, the resistance depends on the inspiratory flow rate. Monitoring of patient's breathing pattern and flow rate is necessary. The treatment regime suggested is 30 minutes (range = 15-50 min)daily for 4 weeks to 6 months (Reid 1995). Some studies related to its effectiveness as: Dekhuijzen 1991, Belman 1988, Harver 1989. Threshold Loading Patient inspires against a threshold load and breathes out unimpeded. It was documented that varying inspiratory flow rates did not appreciably alter inspiratory pressures, and thus threshold loading devices functioned effectively (Larson JL et al, 1988; Goldstein R et al, 1989) Adequate training stimulus is essential so as to provide a positive effect on inspiratory muscle function. The pressure loads of at least 30% of maximal inspiratory mouth pressure (PImax or MIP) have been suggested (Larson JL et al, 1988; Lisboa C et al, 1994) as a adequate training load. The duration of training was 10 minutes to 1 hour; the frequency of training was 3 times per week to daily, and the time course of training sessions ranged from 4 weeks to 6 months (Reid WD, 1995). Isocapnic hyperventilation(Maximum sustained voluntary ventilation) Isocapnic hyperventilation was introduced in 80s. Patient hyperventilate for 15 to 30 minutes through a rebreathing device to maintain the partial pressure of arterial carbon dioxide (i.e. isocapnia) at a target level. (Ries AL & Moser KM, 1986).The clinical usage of Isocapnic hyperventilation is questionable for its inconvenience and costly. (Reid WD, 1995). Studies

30

supported the effectiveness of the isocapnic hyperventilation for COPD patients include as: Ries AL & Moser KM, 1986; Belman MJ, 1980;Levine S, 1986.The duration of training was usually 15 to 30 minutes per session, the frequency of training was 3 to 6 times a week, and the time course of training was 4 to 6 week (Reid WD, 1995). .

- Dekhuijzen PNR, Folgering HTM, van Herwaarden CIA 1991. Target flow inspiratory muscle training during pulmonary rehabilitation in patients with COPD. Chest 99: 128-133.)

- Belman MJ, Shadmehr R 1988. Targeted resistive ventilatory muscle training in chronic obstructive pulmonary disease. J Appl Physiol 65: 2726-2735.

- Harver A, mahler DA, Daubenspeck JA 1989. Targeted inspiratory muscle function and reduces dyspnea in patients with chronic obstructive pulmonary disease. Ann Intern Med 111: 117-124.

- Larson JL, Kim MJ, Sharp JT, et al (1988). Inspiratory muscle training with a pressure threshold breathing device in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. 138:689-696.

- Goldstein R, De Rosie J, Long S, et al (1989). Applicability of a threshold loading device for inspiratory muscle training in patients with COPD. Chest 96: 564-571.

- Lisboa C, Munoz V, Beroiza T, Leiva A,Cruz E (1994). Inspiratory muscle training in chronic airflow limitation: comparison of two different training loads with a threshold device. Eur Respir J. 7: 1266-74.

- Reid WD, Samral B(1995). Respiratory muscle training for patients with chronic obstructive pulmonary disease. Physical Therapy 75(11): 996-1006).

- Ries AL, Moser KM (1986). Comparison of isocapnic hyperventilation and walking exercise training at home in pulmonary rehabilitation. Chest 90(2): 285-289

- Belman MJ, Mirtman C (1980). Ventatory muscle training improves exercise capacity in chronic obstructive pulmonary disease patients. Am Rev Respir Dis 121: 273-280.

- Weiser P, Gillen J(1986). Evaluation of a ventilatory muscle endurance training program in the rehabilitation of patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 133: 400-406.

31

Appendix VI: Six Minutes Walk Test

Equipment Method to measure walking distance (e.g., rolling distance marker); ideal walking distance at least 100 feet in length with minimal traffic; stopwatch; cutaneous pulse oximeter; copy of the 10-point Borg scale in large print; sphygmomanometer; stethoscope; a walker, cart, or wheelchair for patients who require supported walking (e.g., patients with severe dyspnea or orthopedic conditions, etc.); chairs to be positioned along the walking course to be used if needed. Procedure: 1. Prior to the walk test following information may be documented: blood pressure, pulse,

oxyhemoglobin saturation, dyspnea level (show patient 10-point Borg Scale), medications, oxygen, and assistive devices. Patients who use prescribed medications prior to exercise/activity (e.g., inhaled beta agonist, nitroglycerin) should do so before performing the test. Also patients who use oxygen with exercise/ activity should do so during the test at their prescribed liter flow. The portable oxygen equipment may be carried by the staff, or it may be placed in a cart or wheelchair for the patient to push as determined by the patient's individual needs. The walker, cart, or wheelchair may also be used for the patients who require supported walking.

2. If a team member accompanies the patient during the test, that member should walk behind the patient so that she does not influence the patient's pace. During the test the team member may provide words to encouragement (e.g., "you're doing great." "keep up the good work," "hang in there").

3. Oxyhemoglobin saturation should be assessed continuously during the test. Patients who desaturate to levels below 88% may be allowed to continue the test if severe symptoms are not present (e.g., increased dyspnea, chest pain). Realize that some patients may enter the pulmonary rehabilitation program with severe hypoxemia who have been functioning with these levels at home. The urgency to stop the test, therefore, may not be warranted unless the patient is experiencing significant symptoms. We want to document what is truly happening to the patient at home. If oxygen therapy is ordered and initiated these patients may then be retested.

4. Documentation during the walk test may include oxyhemoglobin saturation, heart rate, dyspnea level, patient symptoms and comments, and frequency and length of rest periods.

5. Documentation post walk test may include oxygenhomoglobin saturation; heart rate; blood pressure; dyspnea level; symptoms; patient and team member comments: if test was performed on room air or with oxygen (document liter flow); if patient required supported walking via a cart, walker, or wheelchair. The total time for the test is 6 or 12 minutes, which includes any rest stops. Example: Patient performed a 6-minute walk test and rested twice for 30 seconds each, for a total rest time of 1 minute. Patient walked 5 minutes of the 6-minute test and covered a total distance of 1,050 feet.

6. The following instructions should be given to the patients: "The purpose of this test is to assess your exercise ability and to obtain a baseline of information (i.e., oxygen saturation, dyspnea level, blood pressure, heart rate, and distance

32

walked). You will begin at the designated starting point and follow the walking course as directed, covering as much distance as possible or walking at your own pace in the 6- or 12-minute period. If you need to, you may stop and rest. You will be asked to rate your dyspnea level during the walk test and told to stop when the 6 or 12 minutes are up. To save your breath for the test do not carry on a conversation while walking." Patients should then be asked to repeat the instructions to verify that they understand them.

7. If two walk tests are performed, at least 10-15 minutes of rest between each test is advised. Another option is to perform the tests on separate days. Adapted from "Exercise Assessment and Training" by American Association of Cardiovascular & Pulmonary Rehabilitation, 1998. In Guidelines for Pulmonary Rehabilitation Programs, 2nd ed. (Champaign: Human Kinetics), p58.

33

Further Readings Some major cited documents are attached as soft files in the floppy for references: 1. AARC Clinical Practise Guideline 1.1 Use of Positive Airway Pressure Adjuncts to Bronchial Hygiene Therapy 1.2 Postural Drainage Therapy 1.3 Directed Cough 2. Cochrane Reviews 2.1 Bronchopulmonary hygiene 2.2 Acupunture on chronic asthma 2.3 Domiliary Oxygen 3. Reviews/Guidelines 3.1 ACCP/AACVPR Pulmonary Rehabilitation Guidelines