Definition:
Chronic bronchitis is a chronic or recurrent increase in the volume of mucus secretion sufficient to cause expectoration when this is not due to localized bronchopulmonary disease. In the definition of this disease, chronic/recurrent is further defined as a daily cough with sputum for at least 3 months of the year for at least two consecutive years and airways obstruction which does not change markedly over periods of several months (West 1995). Chronic bronchitis is a clinical diagnosis (unlike the definition of emphysema).
Aetiology of Chronic Bronchitis
This
is more common in middle to late adult life and in men more than women (Clarke
1991). Cigarette smoking is the chief culprit, and although in the UK over 20%
of the adult population continue to smoke
(Department
of Health 1997) only 15-20% of smokers develop COPD. The reason for this is
probably genetic although the number of cigarettes smoked does have an effect
on the progression of the disease.
Exposure to risk:
pack-years
Rather
than simply recording a patient's current smoking habits, a much better indicator
of any potential deterioration in lung function is an assessment of pack-years,
which is the number of packs (20 per pack) smoked daily multiplied by the
number of years of smoking. For example, someone aged 60 years who has smoked
five cigarettes per day (0.25 of a pack) since the age of 15 has a lifetime exposure
equal to 0.25 x 45 = 11 pack-years. Another person of the same age who smoked
30 cigarettes per day (1.5 packs) between the ages of 15 and 25 (gave up till
age 40, since then has smoked one pack per day) has a lifetime exposure of (1.5
x 10) + (1 x 20) = 35 pack-years.
Atmospheric
pollution (e.g. industrial smoke, smog and coal dust) will also predispose to
the development
of
the disease, which is therefore more common in urban than in rural areas. It is
more prevalent in socioeconomic
groups
4 and 5 and is costly in terms of working days lost annually in Britain.
Pathology of Chronic Bronchitis
The
hallmark is hypertrophy of, and an increase in number of, mucous glands in the
large bronchi and evidence of inflammatory changes in the small airways (Thurlbeck
1976). Some irritative substance stimulates overactivity of the mucus-secreting
glands and the goblet cells in the bronchi and in the bronchioles which causes
secretion of excess mucus. This mucus coats the walls of the airways and tends
to clog the bronchioles, which is functionally more important. The cells increase
in size and their ducts become dilated and may occupy as much as two-thirds of
the wall thickness (West 1995). The airways become narrowed and show inflammatory
changes, which results in mucosal oedema thus further decreasing the diameter
of the airways. The ciliary action is also inhibited. This narrowing of the
lumen of the airways is further emphasised during expiration by the normal shortening
and narrowing of the airways. Consequently the airways obstruction is enhanced
during expiration, with resulting trapping of air in the alveoli. The lungs
gradually lose their elasticity as the disease progresses. They will gradually
become distended permanently, which eventually may cause
extensive
rupture of the alveolar walls. After repeated exacerbations due to infection
there is widespread damage to the bronchioles and the alveoli with fibrosis and
kinking occurring as well as compensatory overdistension of the surviving
alveoli. This is closely allied to and contributory to the development of emphysema.
Clinical Features of Chronic
Bronchitis
The
most important clinical features are cough, sputum, wheeze and dyspnoea.
Cough
The
patient will complain of a cough for many years, initially intermittent and
gradually becoming continuous. Fog, damp or infection increases it. The patient
may also complain of bouts of coughing occasionally on lying down or in the
morning. The cough and sputum production are not associated with either
mortality or disability, and are reversible in most smokers once they stop
smoking. The cough is caused by either irritation of airway nerve receptors due
to the release of compounds from inflammatory cells or from the presence of
increased mucous production.
Sputum
This
is mucoid and tenacious, usually becoming mucopurulent during an infective
exacerbation.
Wheeze
Wheezing
is a symptom described by as many as 80% of patients with COPD. Wheezing is a
characteristic
feature
of COPD, although it is also reported in many other acute and chronic
respiratory diseases. Wheezing
is
caused by the sound generated by turbulent airflow through the narrowed
conducting airways and may be
worse
in the mornings or may be related to weather changes.
Dyspnoea or shortness of breath
This
occurs in patients with COPD and, together with the energy-requiring
consequences of chronic infection
and
inflammation, leads to increased work of breathing (Donahoe et al. 1989). The
patient becomes progressively more short of breath as the disease progresses.
Other
signs and symptoms
Exercise intolerance
Owing
to abnormalities of respiratory function, patients with COPD ventilate
excessively and ineffectively at all work levels compared with subjects with normal
lung function. This limits exercise performance. Limitation of exercise
tolerance is, however, determined not only by pulmonary function but also by
many other factors - including motivation, muscle mass and nutritional status.
Of equal importance is the impact these symptoms have on the patient's quality
of life, activities of daily living and recreational activities. Patients
should also be assessed for the impact that these symptoms have on:
•
ability to work
•
psychological well-being
•
sexual function.
Deformity
These
patients often develop a barrel chest due to hyperinflation and use of accessory
muscles of respiration. The thoracic movements are gradually diminished and
paradoxical indrawing in the intercostals spaces may develop.
Cyanosis
This
is a blue coloration of the skin caused by the presence of desaturated
haemoglobin due to reduced gaseous exchange. Cyanosis is also related to the
development of complications, such as poor cardiac output due to ventricular
failure leading to increased peripheral oxygen extraction. Cyanosis may also be
due to an increase in red blood cells (polycythaemia) in response to chronic
hypoxaemia.
Cor pulmonale
This
may occur in the later stages of COPD. The impaired gas exchange in COPD caused
by the disruption of ventilation and perfusion and the resulting hypoxia leads
to widespread hypoxic pulmonary vasoconstriction.
This
leads to an increase in pulmonary vascular resistance resulting in pulmonary
hypertension (Vender 1994). The increase in the pressure within the pulmonary
artery will create a resistance, which the right ventricle must overcome. This
eventually leads to hypertrophy and dilatation, a condition known as 'cor pulmonale'.
Right
heart failure leads to an increased pressure in the peripheral tissues resulting
in the development of peripheral oedema. The combination of renal hypoxia and
the increase in blood viscosity from polycythaemia increases the systemic blood
pressure (BP) and eventually leads to left heart failure. The development of
pulmonary oedema, which exacerbates the hypoxia and low cardiac output in
patients with COPD, leads to a terminal stage of the disease. The mechanism of
this cycle is illustrated in Figure 14.1.
Lung function
There
is reduction of FEV1 and the forced
vital capacity (FVC) is grossly reduced. The residual volume (RV)
will
be increased at the expense of the vital capacity (VC) because of air trapping
and the inability of the
expiratory
muscles to decrease the volume of the thoracic cavity. The expiratory
flow-volume curve is grossly abnormal in severe disease; after a brief interval
of moderately high flow, flow is strikingly reduced as
the airways collapse, and flow limitation by dynamic compression occurs. A scooped-out appearance is often seen.
Blood gases
Ventilation/perfusion
mismatch is inevitable in COPD and leads to a low arterial oxygen pressure (PaO2)
with or without retention of carbon dioxide (CO2). As the disease becomes
severe, the arterial carbon dioxide pressure (PaCO2) may rise, and there is
some evidence that the sensitivity of the respiratory centre to CO2 is reduced
(Fleetham et al. 1980), which may leave the respiratory stimulus dependent upon
the hypoxic drive. However, more recent evidence suggests that the
administration
of high levels of oxygen (>70%) in patients with COPD may increase
hypercapnia owing to the reversal of pre-existing regional pulmonary hypoxic
vasoconstriction, resulting in greater dead space (Crossley et al. 1997).
Auscultation signs
There
will be inspiratory and expiratory wheeze with added coarse crepitations. The
breath sounds are vesicular with prolonged expiration.
X-ray signs
No
characteristic abnormality is seen in the early stages of the disease. If there
is significant airways obstruction
there
may be signs of chest over-expansion (flattening of the diaphragm) and an
enlarged reterosternal airspace.
MEDICAL TREATMENT OF COPD
Principles of Treatment
1
Decrease the bronchial irritation to a
minimum. The patient should be advised to stop smoking and avoid dusty,
smoky, damp or foggy atmospheres. Occupation or housing conditions may need to
be changed.
2
Control infections. All
infections should be treated promptly as each exacerbation will cause further damage
to the airways. The patient should have a supply of antibiotics at home and receive
a vaccination against influenza each winter. The main affecting organisms are Streptococcus pneumoniae and Haemophilus influenzae, which are
usually sensitive to amoxycillin or trimethoprim.
3
Control bronchospasm. Although
bronchospasm is not a prominent feature of this disease, drugs (e.g. salbutamol)
may be given to relieve the airways obstruction as much as is possible.
4 Control/decrease the amount of sputum. Patients with chronic
bronchitis may present with excessive bronchial secretions and are usually able
to eliminate this by themselves. However, during an episode when secretions may
become difficult to eliminate, physiotherapy techniques including
humidification, positioning and manual techniques may aid expectoration and
reduce airflow obstruction in the short term (Cochrane et al. 1977).
5 Oxygen therapy. Oxygen must be
prescribed and should be given with great care, especially if a normal pH
indicates a chronic compensated respiratory acidosis (renal conservation of
bicarbonate ions (HCO3) to maintain pH within 7.35 to 7.45). In this instance
HCO3 is raised above 24 mmol/L whilst PaO2 is low and the PaCO2 is raised.
Controlled oxygen may be given via a Ventimask (or equivalent) with careful
monitoring of blood gas levels.
6 Long-term oxygen therapy (LTOT).
As respiratory function deteriorates, the level of oxygen in the blood falls
leading to an increase in pulmonary hypoxic vasoconstriction and a
deterioration in cardiac function. In 1981, the Medical Research Working Party examined
the effects of supplementary low-concentrations of oxygen (24%) for 15 hours a
day in COPD and found that it reduced 3- year mortality from 66% to 45%. The
British Thoracic Society guidelines (1997) suggest that patients who have a PaO2
of less than 7.3 kPa, with or without hypercapnia, and a FEVl of less
than 1.5 litres, should receive LTOT. This therapy should be considered also
for patients with a PaO2 between 7.3
and 8.0 kPa and evidence of pulmonary
hypertension, peripheral oedema or nocturnal hypoxia.
Medications
Drugs used in the treatment of
respiratory disease broadly fall into two categories: relievers and preventers.
• The relievers are used to
reduce bronchospasm and include the beta2 agonists (which may be short- or long-acting),
the anticholinergics and the xanthenes derivatives.
• The preventers may be
used to prevent bronchial hyper-reactivity and reduce bronchial mucosal inflammatory
reactions - they include the corticosteroids.
Beta2 (BJ agonists
Beta-agonists such as salbutamol
(Ventolin) and terabutaline (Bricanyl) work by stimulating beta2-receptors, which
are widespread throughout the respiratory system. These stimulate adenylate
cyclase, which leads to bronchodilation. Beta-receptors are also found in other
tissues, including the heart, although these are of the betaj subtype.
Even though modern bronchodilators
are designed to be beta2-selective, they
may still cause an increase in heart rate and other side-effects, which include
fine tremor, tachycardia, hypokalaemia (low potassium) after high doses.
Inhaled therapy is therefore preferred to oral, as the former limits the amount
of drug that finds its way into the general circulation. The long-acting beta-agonist
agents salmeterol and eformoterol offer a more favourable dose regimen, and
respiratory physicians are adding a long-acting beta-agonist for patients who
have not responded fully to short-acting beta-agonists and an anticholinergic
used together.
Anticholinergics
Anticholinergic bronchodilators
work by preventing bronchoconstriction, mediated by the parasympathetic nervous
system. Two agents are currently available, ipratropium bromide and oxitropium
bromide. Most studies suggest that these agents are at least as potent as beta-agonists
when used alone in COPD (Tashkin et al. 1986). A short-acting bronchodilator
(beta2-agonist or anticholinergic)
used 'as required' is recommended as initial therapy in the British Thoracic
Society guidelines (BTS 1997).
Xanthene derivatives
The precise mode of action of the
xanthene derivatives such as theophylline and aminophylline remains somewhat uncertain
although they are moderately powerful bronchodilators. They have, however, been
shown to improve symptoms in COPD by increasing the contractual ability of the
diaphragm (Murciano et al. 1989).
Corticosteroids
The role of inhaled steroids
(beclomethasone, budesonide) in COPD will vary from patient to patient. Steroids
work by reducing inflammation and reducing bronchial hyperactivity. Trials have
shown that about 10-20% of COPD patients will improve significantly following a
short course of high-dose oral steroids (Gross 1995).
The most serious limitation to
oral steroid therapy is the risk of long-term side-effects, which include osteoporosis,
adrenal suppression, muscle wasting, poor immune response and impaired healing.
However, a positive response to
corticosteroids justifies the administration of regular inhaled steroids.
Drug Delivery Systems
The objective of inhaled therapy
in COPD is to maximize the quantity of drug that reaches its site of action
while minimising side-effects from
unintended systemic absorption. Most metered-dose inhalers (which are later
described in detail for asthmatic patients) are designed to deliver particles
of between 0.5 and 10 microns (micrometres). Unfortunately, poor inhaler
technique tends to mean that only a relatively small proportion of the drug
actually reaches its site of action. It is therefore imperative that a good
inhaler technique be adopted (as described for patients with asthma). In acute
exacerbations, when conventional inhalers have proved inadequate, nebulisers
may be used to deliver a therapeutic dose of a drug as an aerosol within a
fairly short period of time, usually 5-10 minutes (British Thoracic Society
1997). The type of nebulizer for home use consists of a compressor or pump, a
chamber and a mask or mouthpiece. The compressor
blows air into the chamber, where
it is forced through a drug solution and past a series of baffles. The solution
is converted into a fine mist, which is then inhaled by the patient through the
mask or the mouthpiece.
PHYSIOTHERAPY TECHNIQUES
General Aims of
Treatment
The general aims are:
• to relieve any bronchospasm and
facilitate the removal of secretions
• to improve the pattern of
breathing, breathing control and the control of dyspnoea
• to teach local relaxation,
improve posture and help allay fear and anxiety
• to increase knowledge of the
patient's lung condition and control of the symptoms
• to improve exercise tolerance
and ensure a longterm commitment to exercise
• to give advice about
self-management in activities of daily living.
The treatment given must be
appropriate to the stage of the disease and the patient's general health.
Removal of secretions
The active cycle of
breathing technique (ACBT)
This is a cycle of breathing
control, thoracic expansion exercises and the forced expiratory technique (FET)
and has been shown to be effective in the clearance of bronchial secretions
(Prior et al. 1979; Wilson et al. 1995) and to improve lung function (Webber et
al. 1986).
Thoracic expansion exercises are
deep breathing exercises (three or four) which may be combined with a 3-second
hold on inspiration (unless the patient is very breathless when this may not be
tolerated). This increase in lung volume allows air to flow via collateral channels
(e.g. the pores of Kohn) and may assist in mobilising the secretions as air is
able to get behind the secretions. The increase in lung volume during the inspiratory
phase of the cycle may also be achieved by the patient performing a 'sniff
manoeuvre at the end of a deep inspiration. Manual techniques, for example shaking,
vibrations or chest clapping, may further aid in removal of secretions.
The FET manoeuvre is a combination
of one or two forced expirations (huffs) against an open glottis (as opposed to
a cough, which is a forced expiration against a closed glottis). An essential
part of the FET manoeuvre is a pause for some breathing control, which prevents
an increase in airflow obstruction.
Postural drainage
This may also aid sputum removal
and may be combined with the ACBT technique. The optimum position for
effectiveness must be established with each individual, although postural
drainage for the lower lobe segments may be difficult as some patients may not
tolerate the head-down position or even lying flat.
Humidification
If the secretions are very thick
and tenacious the patient may be given humidification via a nebuliser. Inhalations
with pine oil added to near-boiling water may also be given prior to treatments
to remove excessive bronchial secretions.
Improving the breathing pattern
The patient is taught how to relax
the shoulder girdle in a supported posturally correct position such as crook half-lying.
Breathing control is taught following clearance of secretions. If the patient
is breathless, respiratory control is regained starting with short respiratory phases
and allowing the rate to slow as the patient's breathing pattern improves.
Increasing/maintaining exercise tolerance
The patient may be treated as an
inpatient or as an outpatient, in a health centre or at home by a community physiotherapist.
It is important to see the patient regularly.
Advice should be given on taking
regular exercises, as for example a short walk every day. If possible, the
patient should be offered participation in a multidisciplinary comprehensive
programme of pulmonary rehabilitation.
There is unequivocal evidence to
suggest that pulmonary rehabilitation improves both exercise capacity and
health-related quality of life (Lacasse et al. 1996). In essence, the
components of a pulmonary rehabilitation programme include aerobic exercise
training, education about the background of the disease, smoking cessation,
compliance with medication, nutritional support and energy-conserving
strategies for activities of daily living (ADLs). Pulmonary rehabilitation programmes
may also include psychosocial support with regard to advice on benefits, sexual
function and anxiety management.
Inspiratory muscle training
The potential for fatigue of the
ventilatory muscles is now recognized as an important component of ventilator limitation
in patients with COPD (Moxham 1990; Green and Moxham 1993). Fatigue may be due
to a combination of:
• increased mechanical load on the
respiratory muscles
• reduced muscle strength
• reduced energy supply to the
respiratory muscles (Roussos and Zakynthinos 1996).
It has also been established that
respiratory muscle weakness, which may be a predisposition to muscle fatigue,
is present in patients with chronic obstructive pulmonary disease (Clanton and
Diaz 1995; Polkey et al. 1995). It therefore follows that training techniques, which
might specifically target the respiratory muscles, may prove beneficial in
patients with COPD who may develop respiratory muscle weakness due to a loss of
muscle mass.
Many studies have been performed
examining the benefits of inspiratory muscle training (IMT), particularly in
patients with chronic obstructive pulmonary disease (Smith et al. 1992). Despite
this intensive investigation, IMT has failed to become part of routine clinical
practice. In part this has been due to the paucity of controlled clinical trials,
but more importantly due to the nature of the training adopted. In general the
trials were confounded by the nature of their training
methodology in which the
frequency, duration and intensity of training were less than that required to achieve
a true training response (Smith et al. 1992).
Therefore the training methodology
employed during IMT should follow the same principles that are applied to other
skeletal muscles in terms of the frequency, duration and intensity of the training.
Training methodologies should also control for the lung volume at which the training
takes place, otherwise the patient may alter the lung volume at which
the training is performed in order
to cope with the resistive load more easily (Goldstein et al. 1993).
However, recent studies which have incorporated these principles during training at 80% of maximum inspiratory pressure (MIP) have shown evidence of muscle fatigue (Chatwin et al. 2000) which indicates an appropriate training response has been applied. Furthermore, by using an appropriate training methodology, increases in exercise capacity in both moderately trained and highly trained subjects and in adult patients with cystic fibrosis have been achieved (Chatham et al. 1999, Enright et al. 2000).
(TIDY'S PHYSIOTHERAPY)
THANK YOU,
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