CHRONIC OBSTRUCTIVE PULMONARY

DISEASE (COPD)

Osmosis Hawler Medical University

College of Medicine
27 slides Department: Internal medicine

Dr. ZAHIR SALIH KHOSHNAW

1 02/01/2022
Osmosis
 Paul bolin

Osmosis-clinic

What is COPD?
l COPD is defined as a preventable and treatable disease
characterised by persistent airflow limitation that is usually
progressive and associated with an enhanced chronic inflammatory
response in the airways and the lungs to noxious particles or gases.

l COPD include chronic bronchitis and emphysema.

l Chronic bronchitis: is a clinical diagnosis. It is defined as a cough
Bronchiectasis
is dilatation
and sputum on most days for more than 3 months of 2 consecutive
and thickening years in the absence of other diseases causing sputum
of airways
proximal to the
production. Osmosis
terminal
bronchioles
l Emphysema: is a pathological diagnosis. There is permanent
enlargement of the airway distal to the terminal bronchioles with
the destruction of alveolar walls.
2 Osmosis
 Onlinemeded

Clinical features
In COPD two classical phenotypes have been
described:
l ‘Pink puffers’(typically thin and breathless, and
maintain a normal PaCO2 until the late stage of
disease)
and
l ‘Blue bloaters’(develop or tolerate hypercapnia earlier
and may develop oedema and secondary
polycythaemia). In practice, these phenotypes often
overlap.
Develop type 2 respiratory
failure with hypoxia and high Ninja nerd
3 PaCO2
 Type I has hypoxemia with normocapnia. Type II has hypoxemia with hypercapnia

The prevalence of COPD

l The prevalence of COPD is directly related to the

prevalence of risk factors in the community, such as:
1. Tobacco smoking( > 10 pack years)
2. Coal dust exposure
3. Use of biomass fuels
4. The age of the population being studied.

l It is predicted that, by 2030, COPD will represent the

seventh leading cause of disability and fourth most
common cause of death worldwide.
 Risk Factors for COPD
Tobacco smoke (95% of cases)
Occupational exposures, such as coal
dust, silica and cadmium
Cannabis smoking
Indoor air pollution: cooking with
biomass fuels
Recurrent childhood infections
Maternal smoking
Genetic
•AATD
Alpha-1 antitrypsin deficiency (AAT
•Airway hyper-reactivity
deficiency) is an inherited condition
that raises your risk for lung and
liver disease. Alpha-1 antitrypsin
(AAT) is a protein that protects the Low birth weigh
lungs. The liver makes it. If the AAT
proteins aren't the right shape, they
get stuck in the liver cells and can't
reach the lungs
Aging Populations
Low socio-economic status
 The pulmonary and systemic features of
chronic obstructive pulmonary disease.

Pulmonary features
1. Chronic cough: May be intermittent and may be unproductive.
2. Dyspnea: Progressive, persistent and characteristically worse
with exercise.
A 55-year-old male had 2 years cough and mucoid
3. Chronic sputum production sputum and scattered ronchi and wheezing. He is a
4. Wheezing chronic smoker. What is his likely diagnosis?

5. Chest tightness a. Chronic Bronchitis.

Systemic features b. Pneumonia.

1. Weight loss
2. Skeletal muscle dysfunction
3. Peripheral oedema
4. Osteoporosis, normal spirometry excludes COPD, but not asthma
5. Depression Explained in osmosis photos
© Disease
 Physical signs:

l Inspection:
1. Barrel-shaped chest ,
2. Using accessory muscles of respiration
3. Expiration through pursed lips
4. Intercostal retraction during inspiration
5. Tripod Position
l Palpation:
1. Decreased cricosternal distance
2. Decreased vocal fremitus
3. Decreased chest expansion
 Physical signs:

•Percussion :
1. Hyperresonant
2. Depressed diaphragm,
3. Diminution of the area of absolute cardiac and liver
dullness. An old age female, thin, pursed lips.
They presented with breathlessness and
chronic cough. Which of the following is

•Auscultation: most specific contributing to his airflow

limitation?

1. Reduced breath sounds a. Increased airway resistance.

2. Prolonged expiration b. Loss of elastic recoil.

3. The presence of wheezing c. Mucus plugs in the small airway.

d. Foreign body in the airway.

4. Crackle can be heard if infection exist.
 1. Which of the following findings on spirometry is diagnostic for emphysema?

a. FEV1/FV less than 70% and FEV predicted less than 70%.

Diagnosis of COPD
SYMPTOMS RISK FACTORS
Tobacco
Shortness of breath
Occupation
Chronic cough
Indoor/outdoor pollution
Sputum
è

SPIROMETRY: Required to establish diagnosis

post-bronchodilator FEV1/FVC < 0.70
© 2017 Global Initiative for Chronic Obstructive Lung Disease
Assessment of severity
 Other Investigations

1. Blood examination (CBC): (anemia or

polycythemia)
2. Sputum examination
1. Streptococcus pneumonia
2. Haemophilus influenzae
3. Moraxella catarrhalis

3. Chest x-ray (hyperinflated chest)

4. High resolution CT scan (emphysema)
differentiate emphysema due to smoking and emphysema due to
AATD.
 Emphysema:-

Centriacinar: associated with smoking

affect upper lobes more

• Panacinar: associated with AATD,

Other Investigations affects the lower lobes more

5. Lung Volumes and Diffusing Capacity: Help to

characterize severity, but not essential to patient
management.
6. Oximetry and Arterial Blood Gases: evaluate
oxygen saturation and need for supplemental oxygen
therapy. The diffusing capacity for carbon monoxide
emphysema destroys alveolar structures, including the gas-exchange surface area

7. Alpha-1 Antitrypsin Deficiency Screening: when

chronic bronchitis COPD develops in patients of Caucasian descent
affects the
conducting
under 45 years or with a strong family history of
airways
COPD.
 surface area through which gas can be exchanged. Conditions not
related directly to lung function can also result in a decreased surface
area available between the alveoli and capillaries

Management

1 - General management
I. Smoking cessation advice
II. Annual influenza vaccination
III. Pneumococcal vaccination
IV. Obesity, poor nutrition, depression and social
isolation should be identified and, if possible,
improved.
V. Mucolytic agents are occasionally used but
evidence of benefit is limited.
Management FEV1 is the amount of air you can force from your lungs in one
second. It's measured during a spirometry test, also known as a
pulmonary function test, which involves forcefully breathing out into
a mouthpiece connected to a spirometer machine

Bronchodilators

l Bronchodilator therapy is central to the management of

breathlessness.
l The inhaled route is preferred.
l Short-acting bronchodilators may be used for patients with mild
disease
l longer-acting bronchodilators are usually more appropriate for those
with moderate to severe disease.
l Significant improvements in breathlessness may be reported despite
minimal changes in FEV1.
l Oral bronchodilator therapy, such as theophylline preparations,
may be contemplated in patients who cannot use inhaled devices
efficiently but their use may be limited by side-effects, unpredictable
metabolism and drug interactions; hence the requirement to monitor
plasma levels.
Management You can use LABAs alone in COPD, but in asthma, they should always be
combined with a glucocorticoid, and in fact, their use alone in asthma
is contraindicated because LABA monotherapy has been associated with
increased incidence of asthma-associated death

Combined inhaled glucocorticoids and

bronchodilators

l The fixed combination of an inhaled glucocorticoid and a LABA:

Long acting beta agonist
– improves lung function
– reduces the frequency and severity of exacerbations
– improves quality of life.

l These advantages may be accompanied by an increased risk of

pneumonia, particularly in the elderly.
l LABA/inhaled glucocorticoid combinations are frequently given with
a long-acting muscarinic antagonist (LAMA).
l LAMAs should be used with caution in patients with significant
heart disease or a history of urinary retention.
Management

Pulmonary rehabilitation

l Exercise should be encouraged at all stages and

patients reassured that breathlessness, while
distressing, is not dangerous.
l Multidisciplinary programmes that incorporate physical
training, disease education and nutritional counselling
reduce symptoms, improve health status and enhance
confidence.
l Most programmes include two to three sessions per
week, last between 6 and12 weeks, and are
accompanied by demonstrable and sustained
improvements in exercise tolerance and health status.
Management

Oral glucocorticoids

l Oral glucocorticoids are useful during exacerbations but

maintenance therapy contributes to osteoporosis and
impaired skeletal muscle function, and should be
avoided.

l Oral glucocorticoid trials assist in the diagnosis of

asthma but do not predict response to inhaled
glucocorticoids in COPD.
Management
Prescription of long-term oxygen
therapy in COPD Imp

l Arterial blood gases are measured in clinically stable

patients on optimal medical therapy on at least two
occasions 3 weeks apart:
–1 PaO2 < 7.3 kPa (55 mmHg) irrespective of PaCO2 and FEV1 <
1.5 L
2
– PaO2 7.3–8 kPa (55–60 mmHg) plus pulmonary hypertension,
peripheral oedema or nocturnal hypoxaemia
–3 the patient has stopped smoking

l Use at least 15 hrs/day at 2–4 L/min to achieve a PaO2

> 8 kPa (60 mmHg) without unacceptable rise in PaCO2
Management

Palliative care

l Addressing end-of-life needs is an important,

yet often ignored, aspect of care in advanced
disease.
l Morphine preparations may be used for
palliation of breathlessness in advanced
disease
l Benzodiazepines in low dose may reduce
anxiety.
Management

Surgical intervention

1 - Bullectomy may be considered when large bullae

compress surrounding normal lung tissue.

2 - Lung volume reduction surgery (LVRS)

l Patients with predominantly upper lobe emphysema,
preserved gas transfer and no evidence of pulmonary
hypertension.
l Both bullectomy and LVRS can be performed
thorascopically, minimising morbidity.

3 - Lung transplantation may benefit carefully selected

patients with advanced disease
21
 ABG analyses showed a PaO 2low PaCO 2high. HCO 3high.

a. Chronic COPD.

12. ABG analyses showed a PaO 2 high PaCO 2 low. HCO 3 low.

a. Exacerbation of COPD
Respiratory acidosis indicates acute respiratory
failure warranting consideration for assisted
ventilation.

Prognosis
l The prognosis is inversely related to age and directly
related to the post-bronchodilator FEV1.
l Additional poor prognostic factors are weight loss and
pulmonary hypertension.
l A composite score (BODE), comprising the body mass
index (B), the degree of airflow obstruction (O), a
measurement of dyspnoea (D) and exercise capacity
(E) may assist in predicting death from respiratory and
other causes.
l Respiratory failure, cardiac disease and lung cancer
represent common modes of death.
Acute exacerbations of COPD
– Acute exacerbations of COPD are characterised by an
increase in symptoms and deterioration in lung function and
Acute
health exacerbations of COPD
status.
– Usually triggered by bacteria, viruses or a change in air
quality.
– They may be accompanied by the development of
respiratory failure and/or fluid retention and represent an
important cause of death.
– Many patients can be managed at home.
– The presence of cyanosis, peripheral oedema or an
alteration in consciousness should prompt referral to
hospital.
– Consideration of comorbidity and social circumstances may
influence decisions regarding hospital admission.
patient had Exacerbation of COPD. PaO2 was high, PCO2 was high. how do you manage?
a. Reduce Oxygen.
b. Non-Invasive Ventilation
 Acute exacerbations of COPD Treatment
Treatment
Treatment
1 - Oxygen therapy
target
pulse
– Controlled oxygen at 24% or 28% should be used with the
oximetry
in these
aim of maintaining a PaO2 of more than 8 kPa (60 mmHg)
patients is (or an SaO2 of more than 90%) without worsening
88% to
92%. acidosis.
2 - Bronchodilators
– Nebulised short-acting β2-agonists combined with an
anticholinergic agent (e.g. salbutamol and ipratropium)
should be administered.
– With careful supervision it is usually safe to drive
nebulisers with oxygen, but if concern exists regarding
oxygen sensitivity, they may be driven by compressed air.
53. A COPD patient. Low PaO2, high PaCO2. What is the
management?

a. 24-28%.
 Acute exacerbations of COPD Treatment
Treatment
3 - Glucocorticoids
– Oral prednisolone reduces symptoms and improves lung
function.
– Doses of 30 mg for 10 days are currently recommended
but shorter courses may be acceptable.
– Prophylaxis against osteoporosis should be considered in
patients who receive repeated courses of glucocorticoids.
4 - Antibiotic therapy
– They are currently recommended for patients reporting an
increase in sputum purulence, sputum volume or
breathlessness.
– In most cases simple regimens are advised, such as an
aminopenicillin, a tetracycline or a macrolide.
– Co-amoxiclav is only required in regions where β-
lactamase-producing organisms are known to be common.
 Treatment
Acute exacerbations of COPD Treatment
5 - Non-invasive ventilation
– Non-invasive ventilation is safe and effective in patients
with an acute exacerbation of COPD complicated by mild
to moderate respiratory acidosis (H+ ≥ 45 nmol/L, pH <
7.35).
– Should be considered early in the course of respiratory
failure to reduce the need for endotracheal intubation,
treatment failure and mortality.
– It is not useful in patients who cannot protect their airway.

6 - Mechanical ventilation
– Mechanical ventilation may be contemplated when there is
a reversible cause for deterioration (e.g. pneumonia) or
when no prior history of respiratory failure has been noted.
 Acute exacerbations of COPD Treatment
7 - Additional therapy
– Exacerbations may be accompanied by the development
of peripheral oedema; this usually responds to diuretics.

– There has been a vogue(acceptance) for using an infusion

of intravenous aminophylline but evidence for benefit is
limited and attention must be paid to the risk of inducing
arrhythmias and drug interactions.

– The use of the respiratory stimulant doxapram has been

largely superseded by the development of NIV but it may
be useful for a limited period in selected patients with a
low respiratory rate.
 Obstructive pulmonary diseases • 573

MEASURE PEAK EXPIRATORY FLOW

Convert PEF to % best or % predicted

Life-threatening/acute 50% Moderate Mild

0% 51% 75% 76% 100%
severe
Arterial blood gas Arterial blood gas Did patient receive nebulised
Nebulised salbutamol 5 mg or therapy before PEF recorded?
Nebulised salbutamol 5 mg or
terbutaline 2.5 mg terbutaline 2.5 mg
Yes No
6–12 times daily or as required Oxygen – high-flow/60%
Oxygen –high-flow/60% Prednisolone 40 mg orally
Usual inhaled
Prednisolone 40 mg orally bronchodilator
(or hydrocortisone 200 mg IV) Wait 30 mins
Wait 60 mins

Measure PEF Home

• Usual treatment
PEF < 60% • Return immediately if worse
Intravenous access, chest X-ray, predicted • Appointment with GP within
plasma theophylline level, plasma K+ 48 hours
Admit
• Administer repeat salbutamol PEF > 60%
5 mg + ipratropium bromide 500 μg predicted
by oxygen-driven nebuliser Home
• Consider continuous salbutamol • Check with senior medical staff
nebuliser 5–10 mg/hr
• Prednisolone 40 mg daily for 5 days
• Consider intravenous magnesium
sulphate 1.2–2.0 g over 20 mins, or • Start or double inhaled
aminophylline 5 mg/kg loading dose glucocorticoids
over 20 mins followed by a • Return immediately if worse
continuous infusion at 1 mg/kg/hr • Appointment with GP within
• Correct fluid and electrolytes 48 hours
(especially K+)

Fig. 17.24 Immediate treatment of patients with acute severe asthma.

17
17.23 Indications for assisted ventilation
in acute severe asthma
• Coma
• Respiratory arrest
• Deterioration of arterial blood gas tensions despite optimal therapy:
PaO2 < 8 kPa (60 mmHg) and falling
PaCO2 > 6 kPa (45 mmHg) and rising
pH low and falling (H+ high and rising)
• Exhaustion, delirium, drowsiness

patient, contributes to delay in delivering appropriate therapy

and to under-treatment.
Prior to discharge, patients should be stable on discharge
medication (nebulised therapy should have been discontinued
for at least 24 hours) and the PEF should have reached 75%
of predicted or personal best. The acute attack should prompt
a look for and avoidance of any trigger factors, the delivery of
asthma education and the provision of a written self-management
plan. The patient should be offered an appointment with a GP or
asthma nurse within 2 working days of discharge, and follow-up
at a specialist hospital clinic within a month.

Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is defined as a
preventable and treatable disease characterised by persistent
airflow limitation that is usually progressive and associated with
an enhanced chronic inflammatory response in the airways
574 • RESPIRATORY MEDICINE

and the lung to noxious particles or gases. Exacerbations and
co-morbidities contribute to the overall severity in individual
patients. Related diagnoses include chronic bronchitis (cough
and sputum for at least 3 consecutive months in each of 2
consecutive years) and emphysema (abnormal permanent
enlargement of the airspaces distal to the terminal bronchioles,
accompanied by destruction of their walls and without obvious
fibrosis). Extrapulmonary effects include weight loss and skeletal
muscle dysfunction (Fig. 17.25). Commonly associated co-morbid
conditions include cardiovascular disease, cerebrovascular
disease, the metabolic syndrome (p. 730), osteoporosis,
depression and lung cancer.
The prevalence of COPD is directly related to the prevalence
of risk factors in the community, such as tobacco smoking,
coal dust exposure or the use of biomass fuels, and to the age
of the population being studied. Those with the most severe
disease bear the greatest personal impact of the condition and
contribute to its significant social and economic consequences
on society. It is predicted that, by 2030, COPD will represent
the seventh leading cause of disability and fourth most common
cause of death worldwide.
Risk factors are shown in Box 17.24. Cigarette smoking
represents the most significant risk factor for COPD and the
risk of developing the condition relates to both the amount and
duration of smoking. It is unusual to develop COPD with less
than 10 pack years (1 pack year = 20 cigarettes/day/year) and
not all smokers develop the condition, suggesting that individual
susceptibility factors are important.
Pathophysiology
COPD has both pulmonary and systemic components (Fig. 17.25).
The presence of airflow limitation combined with premature
airway closure leads to gas trapping and hyperinflation, adversely
affecting pulmonary and chest wall compliance. Pulmonary
hyperinflation also results, which flattens the diaphragmatic
muscles and leads to an increasingly horizontal alignment of
the intercostal muscles, placing the respiratory muscles at a
mechanical disadvantage. The work of breathing is therefore
markedly increased – first on exercise, when the time for expiration
is further shortened, but then, as the disease advances, at rest.
17.24 Risk factors for development of chronic
obstructive pulmonary disease
Environmental factors
• Tobacco smoke: accounts for 95% of cases in the UK
• Indoor air pollution: cooking with biomass fuels in confined areas in
developing countries
• Occupational exposures, such as coal dust, silica and cadmium
• Low birth weight: may reduce maximally attained lung function in
young adult life
• Lung growth: childhood infections or maternal smoking may affect
growth of lung during childhood, resulting in a lower maximally
attained lung function in adult life
• Infections: recurrent infection may accelerate decline in FEV1;
persistence of adenovirus in lung tissue may alter local
inflammatory response, predisposing to lung damage; HIV infection
is associated with emphysema
• Low socioeconomic status
• Cannabis smoking
Host factors
• Genetic factors: α1-antitrypsin deficiency; other COPD susceptibility
genes are likely to be identified
• Airway hyper-reactivity
(FEV1 = forced expiratory volume in 1 sec)

Enlargement of mucus-secreting glands Loss of elastic tissue, inflammation and

and increase in number of goblet cells, fibrosis in airway wall result in premature
accompanied by an inflammatory cell airway closure, gas trapping and dynamic
infiltrate, result in increased sputum hyperinflation leading to changes in
production leading to chronic bronchitis pulmonary and chest wall compliance

Pulmonary vascular Unopposed action of

remodelling and impaired proteases and oxidants
cardiac performance leading to destruction of
alveoli and appearance
of emphysema

Pulmonary
Systemic

Muscular weakness Increased Impaired salt and Altered fat

reflecting deconditioning circulating water excretion metabolism ↑ Prevalence of
and cellular changes inflammatory leading to contributing osteoporosis
in skeletal muscles markers peripheral oedema to weight loss
Fig. 17.25 The pulmonary and systemic features of chronic obstructive pulmonary disease.

A 17.25 Modified Medical Research Council (MRC)
B
Fig. 17.26 The pathology of emphysema. A Normal lung.
B Emphysematous lung, showing gross loss of the normal surface area
available for gas exchange. B, Courtesy of the British Lung Foundation.
Emphysema (Fig. 17.26) may be classified by the pattern of
the enlarged airspaces: centriacinar, panacinar and paraseptal.
Bullae form in some individuals. This results in impaired gas
exchange and respiratory failure.
Clinical features
COPD should be suspected in any patient over the age of
40 years who presents with symptoms of chronic bronchitis
and/or breathlessness. Depending on the presentation, important
differential diagnoses include chronic asthma, tuberculosis,
bronchiectasis and congestive cardiac failure.
Cough and associated sputum production are usually the first
symptoms, and are often referred to as a ‘smoker’s cough’.
Haemoptysis may complicate exacerbations of COPD but should
not be attributed to COPD without thorough investigation.
Breathlessness usually prompts presentation to a health
professional. The level should be quantified for future reference,
often by documenting what the patient can manage before
stopping; scales such as the modified Medical Research
Council (MRC) dyspnoea scale may be useful (Box 17.25). In
advanced disease, enquiry should be made as to the presence
of oedema (which may be seen for the first time during an
exacerbation) and morning headaches (which may suggest
hypercapnia).
Physical signs (p. 546) are non-specific, correlate poorly
with lung function, and are seldom obvious until the disease
is advanced. Breath sounds are typically quiet; crackles may
accompany infection but, if persistent, raise the possibility of
bronchiectasis. Finger clubbing is not a feature of COPD and
should trigger further investigation for lung cancer or fibrosis.
Right heart failure may develop in patients with advanced COPD,
Obstructive pulmonary diseases • 575
dyspnoea scale
Grade Degree of breathlessness related to activities
0 No breathlessness, except with strenuous exercise
1 Breathlessness when hurrying on the level or walking up a
slight hill
2 Walks slower than contemporaries on level ground because
of breathlessness or has to stop for breath when walking at
own pace
3 Stops for breath after walking about 100 m or after a few
minutes on level ground
4 Too breathless to leave the house, or breathless when
dressing or undressing
particularly if there is coexisting sleep apnoea or thromboembolic
disease (‘cor pulmonale’). However, even in the absence of heart
failure, COPD patients often have pitting oedema from salt and
water retention caused by renal hypoxia and hypercapnia. The
term ‘cor pulmonale’ is a misnomer in such patients, as they
do not have heart failure. Fatigue, anorexia and weight loss may
point to the development of lung cancer or tuberculosis, but are
common in patients with severe COPD and the body mass index
(BMI) is of prognostic significance. Depression and anxiety are
also common and contribute to morbidity.
Two classical phenotypes have been described: ‘pink puffers’
and ‘blue bloaters’. The former are typically thin and breathless,
and maintain a normal PaCO2 until the late stage of disease.
The latter develop (or tolerate) hypercapnia earlier and may
develop oedema and secondary polycythaemia. In practice,
17
these phenotypes often overlap.
Investigations
Although there are no reliable radiographic signs that correlate
with the severity of airflow limitation, a chest X-ray is essential
to identify alternative diagnoses such as cardiac failure, other
complications of smoking such as lung cancer, and the presence
of bullae. A blood count is useful to exclude anaemia or document
polycythaemia, and in younger patients with predominantly basal
emphysema α1-antitrypsin should be assayed.
The diagnosis requires objective demonstration of airflow
obstruction by spirometry and is established when the post-
bronchodilator FEV1/FVC is < 70%. The severity of COPD may be
defined in relation to the post-bronchodilator FEV1 (Box 17.26).
Measurement of lung volumes provides an assessment of
hyperinflation. This is generally performed by helium dilution
technique (p. 515); however, in patients with severe COPD, and
in particular large bullae, body plethysmography is preferred
because the use of helium may under-estimate lung volumes.
The presence of emphysema is suggested by a low gas transfer
(p. 515). Exercise tests provide an objective assessment of
exercise tolerance and provide a baseline on which to judge the
response to bronchodilator therapy or rehabilitation programmes;
they may also be valuable when assessing prognosis. Pulse
oximetry may prompt referral for a domiciliary oxygen assessment
if less than 93%.
The assessment of health status by the St George’s Respiratory
Questionnaire (SGRQ) is commonly used for research. In practice,
the COPD Assessment Test and the COPD Control Questionnaire
are easier to administer. HRCT is likely to play an increasing
role in the assessment of COPD, as it allows the detection,
576 • RESPIRATORY MEDICINE

17.26 Spirometric classification of COPD severity FEV1 Never smoked or not

(% of value at age 25) susceptible to smoke
based on post-bronchodilator FEV1
100
Severity of airflow obstruction
post-bronchodilator
NICE Clinical 75
PD FEV1/ FEV1% ATS/ERS GOLD Guideline
FVC predicted (2004) (2008) 101 (2010) Smoked regularly Stopped
< 0.7 ≥ 80% Mild Stage I – Stage I – and susceptible smoking
50 at 45
mild mild1 to its effects
< 0.7 50–79% Moderate Stage II – Stage II –
moderate moderate 25 Stopped
Disability
< 0.7 30–49% Severe Stage III – Stage III – smoking
severe severe at 65
Death
< 0.7 < 30% Very Stage IV – Stage IV – 0
25 50 75
severe very severe2 very severe2 Age (years)
1
Mild COPD should not be diagnosed on lung function alone if the patient is Fig. 17.28 Model of annual decline in FEV1 with accelerated decline
asymptomatic. 2Or FEV1 < 50% with respiratory failure. in susceptible smokers. When smoking is stopped, subsequent loss is
(ATS/ERS = American Thoracic Society/European Respiratory Journal; FEV1 = similar to that in healthy non-smokers. (FEV1 = forced expiratory volume in
forced expiratory volume in 1 sec; GOLD = Global Initiative for Chronic 1 second)
Obstructive Lung Disease; PD = post-bronchodilator)
Adapted from National Institute for Health and Care Excellence (NICE) CG101
– Chronic obstructive pulmonary disease in over 16s: diagnosis and
management; 2010.
smokers, and cessation (p. 94) remains the only strategy that
impacts favourably on the natural history of COPD. Complete
cessation is accompanied by an improvement in lung function
and deceleration in the rate of FEV1 decline (Fig. 17.28). In
regions where the indoor burning of biomass fuels is important,
the introduction of non-smoking cooking devices or alternative
fuels should be encouraged.

R breathlessness. The inhaled route is preferred and a number of
L
Fig. 17.27 Gross emphysema. High-resolution computed tomogram
showing emphysema, most evident in the right lower lobe.
characterisation and quantification of emphysema (Fig. 17.27)
and is more sensitive than the chest X-ray at detecting bullae. It
is also used to guide lung volume reduction surgery.
Assessment of severity
The severity of COPD has traditionally been defined in relation to
the FEV% predicted. However, assessing the impact of COPD
on individual patients in terms of the symptoms and limitations in
activity that they experience and whether they suffer frequent or
significant exacerbations may provide a more clinically relevant
assessment and help guide management.
Management
The management of COPD focuses on improving breathlessness,
reducing the frequency and severity of exacerbations, and
improving health status and prognosis.
Reducing exposure to noxious particles and gases
Sustained smoking cessation in mild to moderate COPD is
accompanied by a reduced decline in FEV1 compared to persistent
Bronchodilators
Bronchodilator therapy is central to the management of
different agents delivered by a variety of devices are available.
Choice should be informed by patient preference and inhaler
assessment. Short-acting bronchodilators may be used for
patients with mild disease but longer-acting bronchodilators
are usually more appropriate for those with moderate to severe
disease. Significant improvements in breathlessness may be
reported despite minimal changes in FEV1, probably reflecting
improvements in lung emptying that reduce dynamic hyperinflation
and ease the work of breathing. Oral bronchodilator therapy,
such as theophylline preparations, may be contemplated in
patients who cannot use inhaled devices efficiently but their
use may be limited by side-effects, unpredictable metabolism
and drug interactions; hence the requirement to monitor plasma
levels. Orally active, highly selective phosphodiesterase inhibitors
remain under appraisal.
Combined inhaled glucocorticoids and bronchodilators
The fixed combination of an inhaled glucocorticoid and a LABA
improves lung function, reduces the frequency and severity of
exacerbations and improves quality of life. These advantages may
be accompanied by an increased risk of pneumonia, particularly
in the elderly. LABA/inhaled glucocorticoid combinations are
frequently given with a long-acting muscarinic antagonist (LAMA).
LAMAs should be used with caution in patients with significant
heart disease or a history of urinary retention.
Oral glucocorticoids
Oral glucocorticoids are useful during exacerbations but
maintenance therapy contributes to osteoporosis and impaired
skeletal muscle function, and should be avoided. Oral

glucocorticoid trials assist in the diagnosis of asthma but do not
predict response to inhaled glucocorticoids in COPD.
Pulmonary rehabilitation
Exercise should be encouraged at all stages and patients
reassured that breathlessness, while distressing, is not dangerous.
Multidisciplinary programmes that incorporate physical training,
disease education and nutritional counselling reduce symptoms,
improve health status and enhance confidence. Most programmes
include two to three sessions per week, last between 6 and
12 weeks, and are accompanied by demonstrable and sustained
improvements in exercise tolerance and health status.
Oxygen therapy
Long-term domiciliary oxygen therapy (LTOT) improves survival in
selected patients with COPD complicated by severe hypoxaemia
(arterial PaO2 < 7.3 kPa (55 mmHg); Box 17.27). It is most
conveniently provided by an oxygen concentrator and patients
should be instructed to use oxygen for a minimum of 15 hours/
day; greater benefits are seen in those who use it for more than
20 hours/day. The aim of therapy is to increase the PaO2 to at
least 8 kPa (60 mmHg) or SaO2 to at least 90%. Ambulatory
oxygen therapy should be considered in patients who desaturate
on exercise and show objective improvement in exercise capacity
and/or dyspnoea with oxygen. Oxygen flow rates should be
adjusted to maintain SaO2 above 90%.
Surgical intervention
Bullectomy may be considered when large bullae compress
surrounding normal lung tissue. Patients with predominantly upper
lobe emphysema, preserved gas transfer and no evidence of
pulmonary hypertension may benefit from lung volume reduction
surgery (LVRS), in which peripheral emphysematous lung tissue is
resected with the aim of reducing hyperinflation and decreasing the
work of breathing. Both bullectomy and LVRS can be performed
thorascopically, minimising morbidity. Lung transplantation may
benefit carefully selected patients with advanced disease (p. 567).
Other measures
Patients with COPD should be offered an annual influenza
vaccination and, as appropriate, pneumococcal vaccination.
Obesity, poor nutrition, depression and social isolation should
be identified and, if possible, improved. Mucolytic agents are
occasionally used but evidence of benefit is limited.
Palliative care
Addressing end-of-life needs is an important, yet often ignored,
aspect of care in advanced disease. Morphine preparations may
be used for palliation of breathlessness in advanced disease and
benzodiazepines in low dose may reduce anxiety. Decisions
regarding resuscitation should be addressed in advance of
critical illness.
17.27 Prescription of long-term oxygen therapy
in COPD
Arterial blood gases are measured in clinically stable patients on
optimal medical therapy on at least two occasions 3 weeks apart:
• PaO2 < 7.3 kPa (55 mmHg) irrespective of PaCO2 and FEV1 < 1.5 L
• PaO2 7.3–8 kPa (55–60 mmHg) plus pulmonary hypertension,
peripheral oedema or nocturnal hypoxaemia
• the patient has stopped smoking
Use at least 15 hrs/day at 2–4 L/min to achieve a PaO2 > 8 kPa
(60 mmHg) without unacceptable rise in PaCO2
Obstructive pulmonary diseases • 577
17.28 Calculation of the BODE index
Points on BODE index
Variable 0 1 2 3
FEV1 ≥ 65 50–64 36–49 ≤ 35
Distance walked in ≥ 350 250–349 150–249 ≤ 149
6 mins (m)
MRC dyspnoea scale* 0–1 2 3 4
Body mass index > 21 ≤ 21
A patient with a BODE score of 0–2 has a mortality rate of around
10% at 52 months, whereas a patient with a BODE score of 7–10 has
a mortality rate of around 80% at 52 months.
*See Box 17.25.
(BODE – see text; FEV1 = forced expiratory volume in 1 sec)
Prognosis
COPD has a variable natural history but is usually progressive.
The prognosis is inversely related to age and directly related
to the post-bronchodilator FEV1. Additional poor prognostic
indicators include weight loss and pulmonary hypertension.
A composite score (BODE), comprising the body mass index
(B), the degree of airflow obstruction (O), a measurement of
dyspnoea (D) and exercise capacity (E) may assist in predicting
death from respiratory and other causes (Box 17.28). Respiratory
failure, cardiac disease and lung cancer represent common
modes of death.
Acute exacerbations of COPD 17
Acute exacerbations of COPD are characterised by an increase
in symptoms and deterioration in lung function and health status.
They become more frequent as the disease progresses and are
usually triggered by bacteria, viruses or a change in air quality.
They may be accompanied by the development of respiratory
failure and/or fluid retention and represent an important cause
of death.
Many patients can be managed at home with the use
of increased bronchodilator therapy, a short course of oral
glucocorticoids and, if appropriate, antibiotics. The presence of
cyanosis, peripheral oedema or an alteration in consciousness
should prompt referral to hospital. In other patients, consideration
of comorbidity and social circumstances may influence decisions
regarding hospital admission.
Oxygen therapy
In patients with an exacerbation of severe COPD, high
concentrations of oxygen may cause respiratory depression
and worsening acidosis (p. 566). Controlled oxygen at 24%
or 28% should be used with the aim of maintaining a PaO2 of
more than 8 kPa (60 mmHg) (or an SaO2 of more than 90%)
without worsening acidosis.
Bronchodilators
Nebulised short-acting β 2 -agonists combined with an
anticholinergic agent (e.g. salbutamol and ipratropium) should
be administered. With careful supervision it is usually safe to
drive nebulisers with oxygen, but if concern exists regarding
oxygen sensitivity, they may be driven by compressed air and
supplemental oxygen delivered by nasal cannula.
578 • RESPIRATORY MEDICINE

Glucocorticoids
Oral prednisolone reduces symptoms and improves lung function.
Doses of 30 mg for 10 days are currently recommended but
shorter courses may be acceptable. Prophylaxis against
osteoporosis should be considered in patients who receive
repeated courses of glucocorticoids (p. 670).
Discharge
Discharge from hospital may be contemplated once patients are
clinically stable on their usual maintenance medication. Hospital
at-home teams may provide short-term nebuliser loan, improving
discharge rates and providing additional support for the patient.
onchial

Antibiotic therapy
The role of bacteria in exacerbations remains controversial and
there is little evidence for the routine administration of antibiotics.
They are currently recommended for patients reporting an increase
in sputum purulence, sputum volume or breathlessness. In most
cases simple regimens are advised, such as an aminopenicillin,
a tetracycline or a macrolide. Co-amoxiclav is only required in
regions where β-lactamase-producing organisms are known
to be common.

Non-invasive ventilation
Non-invasive ventilation is safe and effective in patients with an
acute exacerbation of COPD complicated by mild to moderate
respiratory acidosis (H+ ≥ 45 nmol/L, pH < 7.35), and should be
considered early in the course of respiratory failure to reduce
the need for endotracheal intubation, treatment failure and
mortality. It is not useful in patients who cannot protect their
airway. Mechanical ventilation may be contemplated when there
is a reversible cause for deterioration (e.g. pneumonia) or when
no prior history of respiratory failure has been noted.

Additional therapy
Exacerbations may be accompanied by the development
of peripheral oedema; this usually responds to diuretics.
There has been a vogue for using an infusion of intravenous
aminophylline but evidence for benefit is limited and attention
must be paid to the risk of inducing arrhythmias and drug
interactions. The use of the respiratory stimulant doxapram has
been largely superseded by the development of NIV but it may
be useful for a limited period in selected patients with a low
respiratory rate.

17.29 Obstructive pulmonary disease in old age

• Asthma: may appear de novo in old age, so airflow obstruction
should not always be assumed to be due to COPD.
• Peak expiratory flow recordings: older people with poor vision
have difficulty reading PEF meters.
• Perception of bronchoconstriction: impaired by age, so an older
patient’s description of symptoms may not be a reliable indicator of
severity.
• Stopping smoking: the benefits on the rate of loss of lung function
decline with age but remain valuable up to the age of 80.
• Metered-dose inhalers: many older people cannot use these
because of difficulty coordinating and triggering the device. Even
mild cognitive impairment virtually precludes their use. Frequent
demonstration and re-instruction in the use of all devices are
required.
• Mortality rates for acute asthma: higher in old age, partly
because patients under-estimate the severity of bronchoconstriction
and also develop a lower degree of tachycardia and pulsus
paradoxus for the same degree of bronchoconstriction.
• Treatment decisions: advanced age in itself is not a barrier to
intensive care or mechanical ventilation in an acute episode of
asthma or COPD, but this decision may be difficult and should be
shared with the patient (if possible), the relatives and the GP.