COPD

Definition:
1. Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and
treatable disease that is characterized by persistent respiratory symptoms and airflow
limitation that is due to airway and/or alveolar abnormalities usually caused by
significant exposure to noxious particles or gases

2 subtypes: chronic bronchitis and emphysema (usually coexist to variable degrees)

A. Chronic Bronchitis
a. Productive cough on most days for at least 3 consecutive months in 2
successive years
b. Obstruction is due to narrowing of the airway lumen by mucosal thickening
and excess mucus
B. Emphysema
a. Dilation and destruction of air spaces distal to the terminal bronchiole
without obvious fibrosis
b. Decreased elastic recoil of lung parenchyma causes decreased expiratory
driving pressure, airway collapse, and air trapping
c. Types
i. Centriacinar (respiratory bronchiole)
1. Typical form seen in smokers, primarily affects upper lung
zones
2. Distension and damage of lung tissue is concentrated around
the respiratory bronchioles, whilst the more distal alveolar
ducts and alveoli tend to be well preserved

ii. Panacinar (all parts of acinus)

1. Accounts for about 1% of emphysema cases.
2. Due to α1-antitrypsin deficiency, primarily affects lower lobes
3. Distension and destruction affect the whole acinus, and in
severe cases the lung is just a collection of bullae. Severe
airflow limitation and V Q A / mismatch occur. α1-
Antitrypsin deficiency is associated with this type of
emphysema
Risk factors
1. Tobacco smoking
2. Indoor air pollution
a. Burning wood & biomass fuels for cooking
3. Occupational exposure
4. Outdoor air pollution
5. Asthma and airway hyper-reactivity
a. asthma may be a risk factor for the development of airflow limitation and
COPD
6. Genetic factors
a. severe hereditary deficiency of alpha-1 antitrypsin (AATD)15
b. the gene encoding
i. matrix metalloproteinase 12 (MMP-12)
ii. glutathione S-transferase
7. Respiratory infections
a. Infections, both viral and bacterial, may contribute to the pathogenesis,
progression of COPD and the bacterial colonisation associated with airway
inflammation
b. Vicious Circle Hypothesis
i. Initiating factors
1. e.g. smoking, childhood respiratory disease
a. Impaired mucociliary clearance
i. Bacterial colonisation
1. Inflammatory response
2. Altered elastase – anti-elastase
balance
3. Increased elastolytic activity
ii. Airway epithelial injury
iii. COPD
ii.
8. Age
a. Elderly
9. Gender
a. Female
10. Low Socioeconomic status

Clinical features

1. Dyspnea
a. Progressively worsening
b. Worsening with exercise
c. Persistent
2. Cough
a. Chronic cough
b. Recurrent wheezing
 c. Chronic sputum production
d. May be intermittent or may be unproductive
3. Recurrent lower respiratory tract infection

Clinical Presentation of Chronic bronchitis & Emphesema

A. Bronchitis (Blue Bloater*)
a. Symptoms
i. Chronic productive cough
ii. Purulent sputum
iii. Hemoptysis
b. Signs
i. Cyanosis (2º to hypoxemia and hypercapnia)
ii. wheezes
iii. Peripheral edema from RVF (cor pulmonale)
iv. Crackles,
v. Prolonged expiration if obstructive
vi. * Frequently obese
B. Emphysema (Pink Puffer*)
a. Symptoms
i. Dyspnea (± exertion)
ii. Minimal cough
iii. Tachypnea
iv. Decreased exercise tolerance
b. Signs
i. *Pink skin
ii. Pursed-lip breathing
iii. Accessory muscle use
iv. Cachectic appearance due to anorexia and increased work of
breathing
v. Hyperinflation/barrel chest,
vi. hyperresonant percussion
vii. Decreased breath sounds
viii. Decreased diaphragmatic excursion

Investigation

A. Diagnostic
a. Spirometry
i. the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the
presence of persistent airflow limitation
1. gradual decrease in FEV1 over time with episodes of acute
exacerbations
B. Investigation
a. Chest X ray
b. ABG
 i. performed in patients with
1. FEV1 < 40% predicted
a. if they have low arterial oxygen saturation (less than
92% on pulse oximetry)
2. with clinical signs of respiratory failure
c. Others
i. Full Blood Count
1. This detects underlying anaemia of chronic diseases
2. Polycythaemia can develop with chronic hypoxaemia
ii. Electrocardiography (ECG)
1. ECG is useful in detecting pulmonary hypertension in
advanced disease and concurrent ischaemic heart disease
C. Additional Investigations
a. Six Minute Walk Test (6MWT)
i. This test measures the distance covered during six minutes and is a
useful test of exercise capacity
ii. Alpha-1 Antitrypsin Deficiency Screening
1. This should be performed in young COPD patients (< 45
years old) or those who have a strong family history of the
disease.
b. Other suggested investigations include fasting plasma glucose, serum
albumin and serum fasting lipids to detect other common comorbidities.

1. Chronic Bronchitis
a. Spirometry
i. Reduced FEV1, FEV1/FVC
ii. Normal TLC
b. Chest X Ray:
i. AP diameter normal
ii. Prominent bronchovascular markings
iii. Enlarged heart with cor pulmonale
2. Emphysema
a. Spirometry
i. Reduced FEV1, FEV1/FVC
ii. TLC (hyperinflation)
iii. RV (gas trapping)
b. CXR
i. Increase AP diameter
ii. Flat hemidiaphragm (on lateral CXR)
iii. Reduced heart shadow
iv. Increased retrosternal space Bullae
v. Reduced peripheral vascular markings

Differential Diagnoses
1. Bronchial asthma
a.
 Asthma COPD

Age of onset Usually early Usually > 40 years old

childhood, but
may have onset at any
age

Smoking history May be non-, ex- or Usually > 10 pack-

current years
smoker

Atopy Often Infrequent

Clinical symptoms Intermittent and Persistent and

variable gradually
progressive worsening

Cough Nocturnal cough or on Morning cough with

exertion sputum

Sputum Infrequent Often

Reversibility of airflow Characteristic of Airflow limitation may

obstruction asthma improve
but never normalises

Exacerbations Common at all levels Increase in frequency

of with
severity except in mild increasing severity of
disease disease
b.
2. Bronchiectasis
3. Congestive heart failure
4. Diffuse parenchymal lung disease
5. Pulmonary tuberculosis
6. Pulmonary vascular disease

*Ongoing Monitoring and Assessment

- COPD patients should be followed up regularly as COPD is usually a progressive
disease with deterioration in clinical symptoms and lung function over time
- Ask about
- Exposure to risk factors especially tobacco smoke. Ask about smoking and
their willingness to stop.
- Pharmacotherapy
- Nicotine replacement therapy (NRT) in the form of
transdermal patches, gums, lozenges and nasal sprays
 - Varenicline
- Bupropion
- Nortriptyline
- Counselling
- from doctors and other health professionals, given either by
individual face-to-face interactions, group interactions or
through telephone or web-based quit smoking services
- Combination of counselling and pharmacotherapy
- *Five Step Programme for Intervention
- ASK
- Systematically identify all tobacco users at every visit
- Implement an office-wide system that ensures that, for
EVERY patient at EVERY clinic visit, tobacco-use
status is queried and documented.
- ADVISE
- Strongly urge all tobacco users to quit in a clear,
strong, and personalised manner.
- ASSESS
- Determine willingness to make a quit attempt.
- Ask every tobacco user if he or she is willing to make
a quit attempt at this time (e.g., within the next 30
days).
- ASSIST
- Aid the patient in quitting.
- Help the patient with a quit plan
- Provide practical counselling
- Provide intra-treatment social support
- Help the patient obtain extra-treatment social
support
- Recommend use of approved pharmacotherapy
except in special circumstances
- Provide supplementary materials.
- ARRANGE
- Schedule follow-up contact, either in person or via
telephone.
- Current symptoms and any new or worsening symptoms to suggest
deterioration in lung function or development of complications. Consider the
presence of concomitant conditions or co-morbidities.
- Physical examination
- to detect complications such as respiratory failure or cor pulmonale and other
co-morbidities
- Body weight and body mass index provide information on the nutritional
status of the patient.
- Investigation
- Spirometry measurement especially if symptoms worsen
- Active smokers and patients with frequent exacerbations are at risk of faster
 decline in lung function.
- Pharmacotherapy and other medical treatment
- Assess the effectiveness of current regimen in controlling symptoms and any
side effects from the medications
- Ensure that patients are taking their medication at the right dose and
frequency and inhaler techniques are correct.
- Issues regarding non-compliance to medications should be addressed.
- Exacerbation history
- The frequency, severity and causes of exacerbations should be recorded.
- Severity can be estimated by the increased need for bronchodilator medication or
systemic glucocorticosteroid requirements
- Hospitalisations should be documented including the duration of stay and any use of
invasive and non-invasive ventilation.
- Patient education. It is important for patients with COPD to understand the nature of
their disease, risk factors for progression and strategies to help minimise symptoms.

Management

1. Acute exacerbation of COPD

a. Defined as an event in the natural course of the disease characterised by a
sustained (lasting 48 hours or more) worsening of the patient’s baseline
dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations,
is acute in onset, and may warrant a change in regular medication
b. Objectives of managing exacerbations of COPD:
i. Relieve symptoms and airflow obstruction
ii. Maintain adequate oxygenation
iii. Treat any comorbid conditions that may contribute to the respiratory
deterioration
iv. Treat any precipitating factor such as infection
c. Causes
i. Exacerbations are associated with an increase in airway inflammation
and are caused mainly by
1. lower respiratory tract infections
a. Haemophilus influenzae
b. Moraxella catarrhalis
c. Streptococcus pneumoniae
d. Viral
e. Pseudomonas
i. The risk factors for Pseudomonas aeruginosa
infection include
1. severe airflow limitation
2. recent hospitalisation (in the last 3
months)
3. frequent administration of antibiotics (4
 courses in the last year)
4. severe AECOPD
5. isolation of Pseudomonas aeruginosa
during a previous AECOPD or
colonisation during the stable period
2. inhalation of pollutants
3. others
a. cold air
b. congestive heart failure
c. pulmonary embolism
d. Clinical diagnosis
i. increased dyspnoea, cough and production of sputum which may
become purulent
ii. Non-specific symptoms such as
1. Lethargy
2. Insomnia
3. Sleepiness
4. depression
iii. and confusion
e. General approach
i. Getting history *reveal possible cause(s) of and precipitating factors
for the exacerbation and concomitant medical illnesses
1. Current symptoms
2. COPD severity - to establish baseline condition before COPD
a. FEV1
b. previous exacerbations
c. hospital admissions especially history of admission
into the (ICU) and receiving invasive or non-invasive
ventilation
d. the presence of complications of COPD
3. *Previous episodes of exacerbation
4. *Recent treatment from doctors
5. the presence of comorbidities
6. previous and current medications
ii. PE
1. To check for severity (identifying the danger signs)
a. Vital signs
i. Pulse Oximetry - need for supplemental
oxygen and response to treatment and to guide
further management
1. Oxygen supplementation should be
given if SpO2 < 90%
b. Tachypneic
c. Respiratory distress
d. Concurrent or underlying CVS disease
i. Cardiac arrhythmia
 1. Tachyarrhythmia
ii. Heart failure
2. Signs of poorer prognosis
a. Confusion
b. reduced conscious level
c. Cachexia
d. respiratory distress
e. Cyanosis
f. evidence of cor-pulmonale
3. Evidence of comorbid conditions
a. Cardiovascular
neurovascular diseases
b. Diabetes mellitus
c. lung cancer.
.
iii. Investigation
1. Urgent (to check his condition + immediate impression /
diagnosis)
a. ABG
i. Note the FiO2
b. Chest X ray
c. FBC
d. Others
i. ECG
2. Other investigation
a. Full blood count
i. Sepsis
ii. Polycythaemia and raised haematocrit levels
suggest cor pulmonale
iii. Anaemia
1. could be due to underlying chronic
disease, malnutrition or blood loss.
b. Renal profile
i. Urea
ii. Creatinine
iii. Electrolyte
iv. *renal impairment, uncontrolled diabetes
c. LFT
i. malnutrition
d. Sputum Gram Stain and Culture
i. In patient
1. Straight away do
ii. Out patient
1. In an outpatient setting, if an AECOPD
is infectious in nature and does not
respond to initial antibiotic therapy,
 sputum culture and sensitivity should
be performed
e. Chest Radiograph
i. To identify possible causes of the AECOPD
1. Pneumonia
ii. alternative diagnoses that may mimic features
of COPD
1. heart failure
2. Bronchiectasisand
iii. possible complications
1. lung cancer
2. Pneumothorax
f. Electrocardiogram (ECG)
i. for the diagnosis of
1. Tachyarrhythmias
2. myocardial ischaemia
3. Right ventricular hypertrophy
*Non-compliance to medications may mimic an exacerbation, therefore careful history
taking is necessary. If patients do not respond to standard therapy, they need to be
reassessed to determine if they have other diagnoses that may imitate or aggravate their
AECOPD such as:
1. Asthma (may coexist with COPD)
2. Bronchiectasis
3. Diffuse parenchymal lung disease
4. Lung cancer
5. Pulmonary embolism
6. Pneumothorax
7. Heart failure.
iv. Management
*In all situations,
- Optimise bronchodilator therapy and other medical therapy
- Refer to specialist if patient’s condition does not improve

1. First line management

a. Oxygen
i. If SPO2 < 90%
ii. Maintain it at 88 - 92%
b. Pharmaco
i. SABA
1. Inhaled
a. Nebuliser (in hospital)
b. Home (MDI or with spacer)
2. Drugs
a. Salbutamol 200-400 µg or
terbutaline 500 µg every 3-4
 hours
ii. short-acting anticholinergic
1. Inhaled
2. Drugs
a. Ipratropium bromide 40 µg 6
hourly
iii. Systemic Corticosteroid
1. used in addition to existing
bronchodilator therapy in an AECOPD
with significant increase in dyspnoea or
if the patient’s baseline FEV1 is < 50%
predicted
2. Systemic corticosteroids have been
shown to
a. shorten recovery time
b. improve oxygenation and lung
function
c. reduce treatment failure
3. Drugs
a. Prednisolone
i. Oral
ii. 30-40 mg prednisolone
OD for 7-14 d
b. Hydrocortisone
i. IV
*In severe exacerbations, intravenous methylxanthines can be considered if there is
inadequate response to inhaled SABA and SAAC
- Intravenous aminophylline is 250-500 mg (5 mg/kg) over 20 minutes followed by a
maintenance dose of 500 µg/kg/hour, adjusted according to plasma theophylline
concentration (10–20 mg/L or 55–110 µmol/L)
- The metabolism of Amitriptyline can be decreased when combined with
Theophylline
iv. Antibiotic
1. Only start when pt Increased purulence
in sputum AND one of the following
a. Increased sputum volume
b. Increased dyspnoea
2. The presence of purulent sputum in
AECOPD is enough to commence
empirical antibiotic therapy
*Antibiotic
1. Outpatient
a. Amoxicillin/clavulanate 625mg PO TDS for 5-7 days
2. Inpatient
a. Amoxycillin/clavulanate 1.2gm IV TDS for 5-7days PLUS/MINUS
Azithromycin 500mg IV/PO for 3-5 day
b. *If suspect Pseudomonas infection
i. **Piperacillin/tazobactam (Zosyn) 4.5g IV q6-8h
ii. Cefepime 2g IV TDS
PLUS/MINUS
iii. Azithromycin 500mg IV/PO for 3-5 days

c. *Assess the response

i. Good response
1. Is there indication for hospital
admission
a. Indications
i. Marked increased in
severity of symptoms
ii. Development of new
physical signs -
cyanosis, peripheral
oedema
iii. Hemodynamically
instability or cardiac
arrhythmia
iv. Failure to response to
initial treatment
v. Underlying severe
COPD
b. Yes
i. Admit to hospital
c. No
i. Discharge the patient
ii. Follow up
iii. Check for inhaler
technique
iv. Home management
- Step up patient original
treatment: increase dose
+ frequency of MDI
- Give oral prednisolone
30 - 40mg OD x 7 -14
days
- Antibiotic (complete the
course if started)
ii. Failure to response
1. Straight hospital admission!
2. Hospital management
a. Same initial treatment
b. Consider Add on aminophylline
if failed response to inhaled
 SABA
c. Systemic corticosteroid 7- 14
days
d. Closely monitor patient
condition
e. Consider invasive / non-
invasive ventilation
i. Contraindication for
NIV
ii. Respiratory arrest
iii. Cardiovascular
instability (hypotension,
arrhythmias, myocardial
infarction)
iv. At high risk for
aspiration
v. Impaired mental status;
uncooperative patient
vi. Significant facial injury
vii. Viscous or copious
secretions
viii. Recent facial or
gastroesophageal
surgery
ix. Fixed nasopharyngeal
abnormalities
x. Burns
xi. Extreme obesity
xii. Underlying intestinal
obstruction.
f. All the time
i. Monitor fluid balance
and nutrition
ii. Consider subcutaneous
heparin - DVT
iii. Identify and treat
associated conditions
(e.g. heart failure,
arrhythmias)
iv. Monitor patient’s
condition closely
*Discharge patient when
1. Inhaled bronchodilator therapy is required not more frequently than every 4 hours
2. Patient, if previously ambulatory, is able to walk across the room
3. Patient is able to eat and sleep without frequent awakening by dyspnoea
4. Patient has been clinically stable for 12-24 hours
 5. ABG or SpO2 have been stable for at least 12-24 hours
6. Patient (or home caregiver) understands the disease and its management (including
correct use of medications) at home
7. Follow-up has been organised.

*Follow up
1. reviewed within 8 weeks after discharge. The following should be assessed
a. Ability to cope in the patient’s usual environment
b. Spirometry measurement
c. Inhaler technique
d. Understanding of recommended treatment regime
e. Smoking status and cessation
f. Need for LTOT and/or home nebuliser (for patient with stage IV COPD)
g. Suitability for pulmonary rehabilitation
h. Vaccination with influenza vaccine with or without pneumococcal vaccine
i. Self-management plans and future monitoring.

2. COPD
a. Aim
i. Improving a patient's symptoms, e.g. dyspnoea, cough and tiredness.
ii. Preventing disease progression
iii. Reducing frequency and severity of exacerbation
iv. Improving quality of life
v. Reducing mortality
vi. Others
1. Improving exercise tolerance
2. Improving lung function and general health
b. Non-pharmacology
i. Patient education -Knowledge
1. Cause
2. disease severity
3. specific symptoms
4. response to therapy
5. other comorbidities
ii. smoking cessation
iii. avoidance of exposure
iv. exercise
v. Vaccination
1. Influenza
a. Reduces the risk of COPD exacerbation.
b. COPD patients with influenza have a significant risk
of requiring hospitalisation.
2. Pneumococcal
 a. 23-valent polysaccharide vaccine (PPV23) is
recommended for patients who are younger than 65
years but with a FEV1 < 40 % predicted (irrespective
of age)
b. WHO - vaccinate all COPD patients at least once in
their lifetime
i. have it repeated ≥ 5 years (with a
maximum of two doses in one’s
lifetime)
c. Pharmacological
i. Main therapy
1. Bronchodilators
a. Inhaled short-acting bronchodilators
i. inhaled short-actingβ2-agonists (SABAs)
1. Salbutamol
a. 200 µg PRN or 4 to 6 hourly
2. Terbutaline
a. 500 µg
3. Fenoterol
a. 200 µg
ii. inhaled short-acting anticholinergics (SAACs)
1. MDI ipratropium bromide
a. 40 µg 6 hourly
iii. combination of inhaled SABA and SAAC
achieves a greater bronchodilator effect than
either one alone
*Combivent® nebuliser
- solution 2.5 mL (ipratropium bromide 500 µg, salbutamol 2.5 mg) 6 hourly

Duovent® nebuliser
- solution 4 mL (ipratropium bromide 500 µg, fenoterol 1.25 mg) 6 hourly.
b. Inhaled long-acting bronchodilators (LABAs is 12
hours or longer as compared to 4 hours in SABAs.)
i. long-acting β2-agonists (LABAs)
1. salmeterol 50 µg BD
2. formoterol 9 µg BD
ii. long-acting anticholinergics (LAACs)
1. Tiotropium
a. 18 µg OD
c. Inhaled LABA and inhaled corticosteroid (ICS)
combination
i. ICS
1. fluticasone 500 µg BD
a. Accuhuler
2. budesonide 400 µg BD
a. Turbuhaler
 ii. *in patients who are already on a LABA/ICS
combination, but still have persistent
symptoms, addition of a LAAC should be
considered
d. Others
i. Methylxanthines
1. Theophylline
a. oral sustained-release
125-300 mg BD
b. weak bronchodilator +
considered as 3rd line therapy
c. narrow therapeutic window and
significant toxicity, monitoring
of drug levels is desirable
i. therapeutic range is 10-
20 mg/L
d. Side effect
i. cardiac arrhythmias
ii. Nausea, vomiting,
diarrhoea
ii. Phosphodiesterase-4 (PDE4) inhibitors
1. roflumilast 500 mg OD
a. Oral
2. cilomilast 15 mg BD
a. Oral
3. Side effect
a. Headache
b. Nausea, vomiting, diarrhoea
2. Management
a. based on
i. disease severity
ii. Symptoms
iii. frequency of COPD exacerbation
b. Severity
i. Mild
ii. Moderate
iii. Severe
iv. Very severe
*Severity of COPD

Stage Severity Classification Classification Other

by post by Dyspnea symptoms
bronchodilator disability
spirometry
values
1 Mild FEV1/FVC < Shortness of Chronic cough
0.70 breath when and sputum
hurrying on the production may
FEV1 > 80% level or walking be present
predicted up a slight hill

2 Moderate FEV1/FVC < Walks slower Dyspnoea

0.70 than people of typically on
the same age on exertion,
50% ≤ FEV1 the level cough and
< 80% because of sputum
predicted breathlessness; production
Or sometimes also
stops for breath present.
after walking
about 100 m or
after a few *the stage at
minutes at own which patients
pace on the usually seek
level medical
attention
because of
chronic
respiratory
symptoms or an
exacerbation of
COPD.

3 Severe FEV1/FVC < Too breathless Greater

0.70 to leave the dyspnoea,
house reduced
30% ≤ FEV1 or breathless exercise
< 50% when dressing capacity,
predicted or fatigue, and
undressing repeated
exacerbations
that almost
always
have an impact
on the patient’s
quality of life.

4 Very severe FEV1/FVC < Presence of Respiratory

0.70 chronic failure may lead
 respiratory to cor
FEV1 < 30% failure or pulmonale with
predicted clinical signs of signs which
right heart include
or failure elevation of the
jugular venous
FEV1 < 50% pressure and
predicted pitting ankle
plus oedema
chronic
respiratory
failure
*FEV1: forced expiratory volume in one second; FVC: forced vital capacity
*Respiratory failure:
- arterial partial pressure of oxygen (PaO2) less than 8.0 kPa (60 mmHg) with or
without
- arterial partial pressure of CO2 (PaCO2) greater than 6.7 kPa (50 mmHg)
while breathing air at sea level.

*Modified Medical Research Council (MMRC) Dyspnoea Scale

Grade Description

0 Not troubled by breathlessness except on strenuous exercise

1 Shortness of breath when hurrying on the level or walking up a

slight hill

2 Walks slower than people of the same age on the level because of
breathlessness or has to stop for breath when walking at own pace
on the level

3 Stops for breath after walking about 100 m or after a few minutes
on the level

4 Too breathless to leave the house or breathless when dressing or

undressing

c. Frequency of symptoms
i. Infrequent
ii. Persistent
1. rescue bronchodilators > 2 per week
iii. Frequent exacerbation (≥ 1 per
yr)
 1. Over past 1 year, 1 or more episodes of
COPD exacerbation requiring
a. systemic corticosteroids
b. antibiotics
c. hospitalisation
d. All COPD patients, irrespective of disease severity,
should be prescribed SABA or SABA/SAAC
combination
e. If mild + infrequent
i. SABA only
f. In any other severity + infrequent
i. SABA/SAAC combination as needed
g. In any other severity + any other frequency
i. ICS/LABA combination
1. +/- LAAC
2. +/- theophylline
a. Theophylline can be added to
patients who are symptomatic
despite maximum inhaled
therapy
h. If respiratory failure (or think of other causes)
i. Long-term oxygen therapy
ii. Consider lung transplantation/LVRS

d. Non-pharmacological Interventions
i. Pulmonary Rehabilitation - last between 6 and 12 weeks
1. Pulmonary rehabilitation should be considered as an addition
to medications for symptomatic patients who have Stage II,
III, or IV COPD
2. Details
a. Focus on muscle of ambulation
i. emphasising endurance and strength training
b. Reversal of muscle deconditioning and better pacing
enables
i. patients to walk further with less dyspnoea
c. *Doesn’t reverse degree of airway obstruction or lung
hyperinflation
3. Benefits
a. Improvement in peripheral muscle strength and mass
b. Improvement in the ability to perform routine
activities of daily living
c. Reduction in number of days spent in hospital
d. Cost effectiveness
ii. Domiciliary Oxygen Therapy
1. *An oxygen concentrator is the most cost-effective method
 for delivering LTOT
2. *Long-term administration of oxygen of > 15 hours per day
3. Indication
a. prescribed for all patients with COPD who have
chronic hypoxaemia
i. PaO2 ≤ 7.3 kPa (55 mmHg) or SaO2 ≤
88%, with or without hypercapnia
ii. PaO2 between 7.3 and 8.0 kPa (55-60 mmHg)
or SaO2 of 89% + there is evidence of
1. Pulmonary hypertension
2. peripheral oedema suggesting
congestive heart failure
3. Polycythaemia (haematocrit > 55%)
4. Not indicated for
a. with severe airflow limitation whose main complaint is
dyspnoea but who maintain a PaO2 > 8 kPa (60
mmHg) and who show no secondary effects of chronic
hypoxia
b. who continue to smoke cigarettes
c. who are not sufficiently motivated to undertake the
discipline required for oxygen therapy.
d. who have not received adequate therapy of other kinds
(eg, inhaled and oral bronchodilators and
corticosteroids, treatment for right ventricular failure
or for any respiratory infection)
5. Patients should be reassessed 1–2 months after starting
continuous or nocturnal oxygen therapy, both clinically and
by measurement of PaO2 and PaCO2
a. After that, reassess annually

*Assessment for LTOT should not be done during an exacerbation or during the recovery
period of an exacerbation.
*Arterial blood gas measurements should be made on two occasions when the patient is in a
stable condition and on optimal treatment
6. Goal
a. To increase the baseline PaO2 to at least 60 mmHg (or
8.0 kPa) at rest, and/or produce an SaO2 of at least
90%.

iii. Nutrition
1. A balanced diet with adequate caloric intake in conjunction
with exercise is recommended in patients with COPD

iv. Lung Volume Reduction

1. Lung Volume Reduction Surgery (LVRS)
 a. Resection of non-functioning emphysematous areas
i. improves exercise tolerance
ii. decreases 2-year mortality in patients with
severe, predominantly upper-lung emphysema
who have low baseline exercise capacity after
pulmonary rehabilitation
2. Bullectomy
a. removal of large bullae compressing on adjacent lung
parenchyma
b. Surgical techniques used have included
i. Thoracotomy
ii. Video-assisted thoracoscopy
iii. stapled wedge resection
3. Minimally-Invasive Lung Volume Reduction Procedures

v. Lung Transplantation
1. limited to younger patients with other chronic lung diseases.
2. Indication
a. When life expectancy is not predicted to exceed 24-36
months despite optimal and maximal medical
management
b. They have class III or IV New York Heart Association
(NYHA) symptoms
c. < 60 years old with an FEV1 < 25% predicted after
bronchodilator therapy or with severe pulmonary
hypertension.

*Surgery in COPD Patients - minimise pulmonary complications in at-risk patients:

1. Preoperative
a. Smoking cessation
b. Optimise COPD treatment regimens
c. Antibiotics for acute bronchitis
d. Educate patient on lung expansion manoeuvre
e. Consider inspiratory muscle training or pulmonary rehabilitation in high-risk
patients
2. Postoperative
a. Early mobilisation
b. Lung expansion manoeuvre
c. consider continuous positive airway pressure (CPAP) in high-risk patients
d. Adequate pain control
i. consider epidural analgesia in at-risk patients
ii. avoid opiates
e. Selective use of nasogastric decompression and total parenteral nutrition
f. Deep vein thrombosis prophylaxis.

Management
1. Non-pharmacological
a. Patient education
b. Smoking Cessation
c. Vaccination
i. Influenza, pneumococcal vaccine
d. eliminate respiratory irritants/allergens (occupational/environmental),
e. exercise rehabilitation to improve physical endurance
2. Pharmacological
a. Symptomatic Relief (no mortality benefit)
i. Bronchodilators (mainstay of current drug therapy, used in
combination
1. Short-acting anticholinergics (e.g. ipratropium bromide) and
short-acting β2-agonists (e.g. salbutamol, terbutaline)
a. SABAs: rapid onset but significant side effects at high
doses (e.g. hypokalemia)

b. Short-acting anticholinergics more effective than

SABAs with fewer side effects but slower onset; take
regularly rather than PRN

2. LABAs (e.g. salmeterol, formoterol, indacaterol) and long-

acting anticholinergics (e.g. tiotropium bromide,
glycopyrronium bromide)
a. More sustained effects for moderate to severe COPD
3. Inhaled corticosteroid (ICS) + LABA combination (e.g.
Advair®: fluticasone + salmeterol, Symbicort®: budesonide +
formoterol)
a. ICS/LABA increases effectiveness vs. LABA alone
4. Others
a. Theophylline:
i. weak bronchodilator; limited evidence to
suggest combination with bronchodilator
ii. Side effects: nervous tremor,
nausea/vomiting/diarrhea, tachycardia,
arrhythmias, sleep changes
b. PDE4 inhibitor: roflumilast (Daxas®) anti-
inflammatory medication useful in COPD with chronic
bronchitis, severe airflow obstruction, frequent
exacerbations.
ii. Corticosteroid
1. ICS monotherapy has been shown to increase the incidence of
pneumonia in COPD;
2. ICS
a. should only be used with a LABA in combination in
patients with a history of exacerbations
iii. Surgical
1. Lung volume reduction surgery (resection of emphysematous
parts of lung, associated with higher mortality if FEV1
<20%), lung transplant