BMJ Best Practice COPD

COPD
The right clinical information, right where it's needed
Last updated: Sep 12, 2019

Table of Contents
Summary 3
Basics 4
Definition 4
Epidemiology 4
Etiology 4
Pathophysiology 4
Prevention 6
Primary prevention 6
Screening 6
Secondary prevention 6
Diagnosis 7
Case history 7
Step-by-step diagnostic approach 7
Risk factors 9
History & examination factors 10
Diagnostic tests 12
Differential diagnosis 14
Diagnostic criteria 15
Treatment 17
Step-by-step treatment approach 17
Treatment details overview 22
Treatment options 26
Emerging 59
Follow up 60
Recommendations 60
Complications 61
Prognosis 62
Guidelines 63
Diagnostic guidelines 63
Treatment guidelines 63
Evidence scores 64
References 66
Images 78
Disclaimer 82
Summary
◊ Progressive disease state characterized by airflow limitation that is not fully reversible.
◊ Suspected in patients with a history of smoking, occupational and environmental risk factors, or a
personal or family history of chronic lung disease.
◊ Presents with progressive shortness of breath, wheeze, cough, and sputum production, including
hemoptysis.
◊ Diagnostic tests include pulmonary function tests, chest x-ray, chest computed tomography scan,
oximetry, and arterial blood gas analysis.
◊ Patients should be encouraged to stop smoking or occupational exposure and be vaccinated against
viral influenza and Streptococcus pneumoniae .
◊ Treatment options include bronchodilators, inhaled corticosteroids, and systemic corticosteroids.
◊ Long-term oxygen therapy improves survival in severe COPD.

COPD Basics
Definition
COPD is a preventable and treatable disease state characterized by airflow limitation that is not fully
reversible. It encompasses both emphysema and chronic bronchitis. The airflow limitation is usually
BASICS
progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or
gases. It is primarily caused by cigarette smoking. Although COPD affects the lungs, it also has significant
systemic consequences. Exacerbations and comorbidities are important contributors to the overall condition
and prognosis in individual patients.[1]
Epidemiology
COPD is more common in older people, especially those ages 65 years and older. Associated mortality in
women has more than doubled over the past 20 years and now matches that in men. The number of COPD
cases in the US has increased by 41% since 1982, and COPD affects 1% to 3% of white women and 4%
to 6% of white men. COPD is projected to be the third leading cause of death in the world by 2020.[1] This
is because of the expanding epidemic of smoking and aging of the world population and reduced mortality
from other causes of death such as cardiovascular disease.[1] [5] A systematic review and meta-analysis has
shown that the prevalence of COPD in adult offspring of people with COPD is greater than population-based
estimates.[6]
Etiology
Tobacco smoking is by far the main risk factor for COPD. It is responsible for 40% to 70% of COPD cases
and exerts its effect by causing an inflammatory response, cilia dysfunction, and oxidative injury. Air pollution
and occupational exposure are other common etiologies. Oxidative stress and an imbalance in proteinases
and antiproteinases are also important factors in the pathogenesis of COPD, especially in patients with
alpha-1 antitrypsin deficiency, who have panacinar emphysema that usually presents at an early age.[1]
Pathophysiology
The hallmark of COPD is chronic inflammation that affects central airways, peripheral airways, lung
parenchyma and alveoli, and pulmonary vasculature. The main components of these changes are narrowing
and remodeling of airways, increased number of goblet cells, enlargement of mucus-secreting glands of the
central airways, and, finally, subsequent vascular bed changes leading to pulmonary hypertension. This is
thought to lead to the pathologic changes that define the clinical presentation.
Evidence suggests that the host response to inhaled stimuli generates the inflammatory reaction responsible
for the changes in the airways, alveoli, and pulmonary blood vessels. Activated macrophages, neutrophils,
and leukocytes are the core cells in this process. In contrast to asthma, eosinophils play no role in COPD,
except for occasional acute exacerbations. However, a patient-level meta-analysis found that patients with
COPD with lower blood eosinophil counts have more pneumonia events than do those with higher counts.[7]
In emphysema, which is a subtype of COPD, the final outcome of the inflammatory responses is elastin
breakdown and subsequent loss of alveolar integrity.[8] In chronic bronchitis, another phenotype of
COPD, these inflammatory changes lead to ciliary dysfunction and increased goblet cell size and number,
which leads to the excessive mucus secretion. These changes are responsible for decreased airflow,
hypersecretion, and chronic cough. In both conditions, changes are progressive and usually not reversible.
4 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Sep 12, 2019.
BMJ Best Practice topics are regularly updated and the most recent version
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subject to our disclaimer. © BMJ Publishing Group Ltd 2020. All rights reserved.
COPD Basics
Increased airway resistance is the physiologic definition of COPD. Decreased elastic recoil, fibrotic changes
in lung parenchyma, and luminal obstruction of airways by secretions all contribute to increased airways
resistance. Expiratory flow limitation promotes hyperinflation. This finding, in addition to destruction of lung
parenchyma, predisposes COPD patients to hypoxia, particularly during activity. Progressive hypoxia causes
BASICS
vascular smooth muscle thickening with subsequent pulmonary hypertension, which is a late development
conveying a poor prognosis.[9] [10]
This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Sep 12, 2019.
5
COPD Prevention
Primary prevention
Avoidance of tobacco exposure (both active and passive measures) and toxic fumes are of invaluable
importance in primary prevention of COPD. All smokers should be offered interventions aimed at smoking
cessation, including pharmacotherapy and counseling. Although smoking cessation may be associated
with minor short-term adverse effects such as weight gain and constipation, its long-term benefits are
unquestionable.[17] For disease due to occupational exposures, primary prevention is achieved by
elimination or reduction of exposures in the workplace.
Screening
There are no data to show conclusively that screening spirometry is effective in directing management
decisions or in improving COPD outcomes in patients who are identified before the development of
significant symptoms.[24] However, if COPD is diagnosed at an early stage and risk factors are eliminated,
the rate of decline in lung function will dramatically decrease. Treatment is much more efficacious in the early
stages of disease.[25]
Screening can be done by asking about smoking history and environmental or occupational exposure. In
PREVENTION
high-risk populations a screening spirometry should be obtained to document airway obstruction. Some
experts advocate conducting screening spirometry in all patients with findings compatible with emphysema
on chest x-ray or computed tomography of the chest. Significant pulmonary dysfunction may be present in
asymptomatic smokers.
Secondary prevention
Vaccination against viral influenza and Streptococcus pneumoniae is strongly recommended in all patients
with cardiopulmonary diseases, including COPD.
Use of calcium and other medication may be necessary to prevent or treat osteoporosis in some patients,
especially older women on long-term corticosteroid therapy. Bone density scans are done to evaluate
progression of this condition.
There are conflicting data with regards to prophylactic antibiotic therapies. Prophylactic antibiotics, such
as macrolides, may be considered for reducing the risk of acute exacerbation.[147] [148] While current
guidelines do not yet advocate the use of prophylactic antibiotics, evidence from the MACRO study
suggests that azithromycin reduces the risk of acute exacerbations in patients with COPD. However, when
administered for 1 year, the most noted side effect was a decrement in hearing.[149] Azithromycin therapy
is believed to be most effective in preventing acute exacerbation with a great efficacy in older patients and
milder Global Initiative for Chronic Obstructive Lung Disease (GOLD) stages. Little evidence of treatment
benefit is seen in current smokers.[114]
Physical activity is recommended for all patients with COPD.[1]
COPD Diagnosis
Case history
Case history #1
A 66-year-old man with a smoking history of 1 pack per day for the past 47 years presents with
progressive shortness of breath and chronic cough, productive of yellowish sputum, for the past 2 years.
On examination he appears cachectic and in moderate respiratory distress, especially after walking to the
examination room, and has pursed-lip breathing. His neck veins are mildly distended. Lung examination
reveals a barrel chest and poor air entry bilaterally, with moderate inspiratory and expiratory wheezing.
Heart and abdominal examination are within normal limits. Lower extremities exhibit scant pitting edema.
Case history #2
A 56-year-old woman with a history of smoking presents to her primary care physician with shortness
of breath and cough for several days. Her symptoms began 3 days ago with rhinorrhea. She reports a
chronic morning cough productive of white sputum, which has increased over the past 2 days. She has
had similar episodes each winter for the past 4 years. She has smoked 1 to 2 packs of cigarettes per day
for 40 years and continues to smoke. She denies hemoptysis, chills, or weight loss and has not received
any relief from over-the-counter cough preparations.
Other presentations
Other presentations include weight loss, hemoptysis, cyanosis, and morning headaches secondary to
hypercapnia. Physical examination may demonstrate hypoxia, use of accessory muscles, paradoxical
rib movements, distant heart sounds, lower-extremity edema and hepatomegaly secondary to cor
pulmonale, and asterixis secondary to hypercapnia. Patients may also present with signs and symptoms
of COPD complications. These include severe shortness of breath, severely decreased air entry, and
chest pain secondary to an acute COPD exacerbation or spontaneous pneumothorax.[2] [3] Patients with
COPD often have other comorbidities, including cardiovascular disease,[4] skeletal muscle dysfunction,
DIAGNOSIS
metabolic syndrome and diabetes, osteoporosis, depression, lung cancer, gastroesophageal reflux
disease, bronchiectasis, and obstructive sleep apnea.[1]
Step-by-step diagnostic approach

History
COPD has an insidious onset and usually presents in older people. A history of productive cough,
wheezing, and shortness of breath, particularly with exercise, is typical. Patients may complain of
fatigue as a result of disrupted sleep secondary to constant nocturnal cough and persistent hypoxia
and hypercapnia. The patient's smoking history, occupational exposures, and any family history of lung
disease should be determined.
Patients with COPD may also present with acute, severe shortness of breath, fever, and chest pain during
acute infectious exacerbation. See our topic on Acute exacerbation of chronic obstructive pulmonary
disease for further information.
7
COPD Diagnosis
Physical exam
Examination may show tachypnea, respiratory distress, use of accessory muscles, and intercostal
retraction. Barrel chest is a common observation. There may be hyperresonance on percussion, and
distant breath sounds and poor air movement on auscultation. Wheezing, coarse crackles, clubbing,
and cyanosis, as well as signs of right-side heart failure (distended neck veins, loud P2, hepatomegaly,
hepatojugular reflux, and lower-extremity edema), may be present. Occasionally patients may exhibit
asterixis - loss of postural control in the outstretched arms (commonly known as a flap) caused by
hypercapnia. This is due to impaired gas exchange in lung parenchyma, worsens with exercise, and is
suggestive of respiratory failure.
Initial tests
Spirometry is the first test for diagnosis of COPD and for monitoring disease progress. Patients with
COPD have a distinctive pattern seen on spirometry, with a reduced FEV1 and FEV1/FVC ratio. The
presence of airflow limitation is defined by the Global Initiative for Chronic Obstructive Lung Disease
(GOLD) criteria as a postbronchodilator FEV1/FVC <0.70.[1] In cases where FVC may be hard to
measure, FEV6 (forced expiratory volume at 6 seconds) can be used.[18] Chest x-ray (CXR) is rarely
diagnostic but can help exclude other diagnoses. Pulse oximetry screens for hypoxia.
In addition to airflow limitation, the GOLD guidelines recognize the importance of exacerbations in
affecting the natural course of COPD, and place emphasis on assessment of symptoms, risk factors for
exacerbations, and comorbidities.[1]
The Modified British Medical Research Council (mMRC) questionnaire or the COPD Assessment Test
(CAT) are recommended to assess symptoms. These can be found in the GOLD guidelines.[1]
The number of previously treated exacerbations (2 or more per year) is the best predictor of having
another exacerbation. In addition to previous exacerbations, airflow limitation <50% is predictive of
exacerbations.
The GOLD guideline uses a combined COPD assessment approach to group patients according to
DIAGNOSIS
symptoms and previous history of exacerbations. Symptoms are assessed using the mMRC or CAT scale.
• Group A: low risk (0-1 exacerbation per year, not requiring hospitalization) and fewer symptoms
(mMRC 0-1 or CAT <10)
• Group B: low risk (0-1 exacerbation per year, not requiring hospitalization) and more symptoms
(mMRC ≥2 or CAT≥ 10)
• Group C: high risk (≥2 exacerbations per year, or one or more requiring hospitalization) and fewer
symptoms (mMRC 0-1 or CAT <10)
• Group D: high risk (≥2 exacerbations per year, or one or more requiring hospitalization) and more
symptoms (mMRC≥ 2 or CAT≥ 10).
Other tests
Detailed pulmonary function tests performed in specialist pulmonary function laboratories can measure
diffusing capacity of the lung for carbon monoxide (DLCO), flow volume loops, and inspiratory capacity.
They are not used routinely but can be helpful in resolving diagnostic uncertainties and for preoperative
assessment.[1]
COPD Diagnosis
In young patients (<45 years) with a family history or with rapidly progressing disease and lower lobe
changes on imaging tests, alpha-1 antitrypsin level should be checked. The World Health Organization
recommends that all patients with a diagnosis of COPD should be screened once, especially in areas with
high prevalence of alpha-1 antitrypsin deficiency.[19] This may aid in family screening and counseling.
Computed tomography scans show anatomic changes, but their usefulness in diagnosis is confined to
patients considered for surgery and for ruling out other pathologies.[1]
Pulse oximetry should be used to assess all patients with clinical signs of respiratory failure or right heart
failure. If peripheral arterial oxygen saturation is less than 92%, then arterial or capillary blood gases
should be measured.[1]
Obstructive sleep apnea is associated with increased risk of death and hospitalization in patients with
COPD.[20]
Exercise testing can be useful in patients with a disproportional degree of dyspnea.[21] It can be
performed on a cycle or treadmill ergometer, or by a simple timed walking test (e.g., 6 minutes, or duration
<6 minutes).[22] Exercise testing is also of use in selecting patients for rehabilitation. Respiratory muscle
function may also be tested if dyspnea or hypercapnia are disproportionately increased with respect to
FEV1, as well as in patients with poor nutrition and those with corticosteroid myopathy.[23]
In patients with frequent exacerbations, severe airflow limitation, and/or exacerbations requiring
mechanical ventilation, sputum should be sent for culture.[1]
[VIDEO: Radial artery puncture animated demonstration ]
Risk factors
Strong
cigaret te smoking
DIAGNOSIS
• Most important risk factor. It causes 40% to 70% of cases of COPD.[11]
• Elicits an inflammatory response and causes cilia dysfunction and oxidative injury.
advanced age
• The effect of age may be related to a longer period of cigarette smoking as well as the normal age-
related loss of FEV1.
genetic factors
• Airway responsiveness to inhaled insults depends on genetic factors. Alpha-1 antitrypsin deficiency
is a genetic disorder, mostly encountered in people of northern European ancestry, which causes
panacinar emphysema in lower lobes at a young age.
Weak
white ancestry
• Despite high rates of smoking among black Americans and other racial and ethnic groups, COPD is
more common in white people.
9
COPD Diagnosis
exposure to air pollution or occupational exposure
• Chronic exposure to dust, traffic exhaust fumes, and sulfur dioxide increases risk of COPD.
developmentally abnormal lung

• Frequent childhood infection may cause scarring of lungs, decrease elasticity, and increase risk for
COPD.
male sex
• COPD is more common in men, but that is probably secondary to more smokers being male. However,
there is a suggestion that women may be more susceptible than men to the effects of tobacco
smoke.[12] [13] [14] [15]
low socioeconomic status

• The risk for developing COPD is increased in people with lower socioeconomic status.[16] However,
this may reflect exposure to cigarette smoke, pollutants, or other factors.
History & examination factors

Key diagnostic factors
cough (common)
• Usually the initial symptom of COPD.
• Frequently a morning cough, but becomes constant as disease progresses.
• Usually productive, and sputum quality may change with exacerbations or superimposed infection.
shortness of breath (common)

• Initially with exercise but may progress to shortness of breath even at rest.
• Patients may have difficulty speaking in full sentences.
DIAGNOSIS
Other diagnostic factors

barrel chest (common)
• The anteroposterior diameter of the chest is increased.
• This suggests hyperinflation and air trapping secondary to incomplete expiration.
hyperresonance on percussion (common)

• Caused by hyperinflation and air trapping secondary to incomplete expiration.
distant breath sounds on auscultation (common)

• Caused by barrel chest, hyperinflation, and air trapping.
poor air movement on auscultation (common)

• Secondary to loss of lung elasticity and lung tissue breakdown.
wheezing on auscultation (common)

• A common finding in exacerbations. The current accepted descriptive word for a continuous musical
lung sound.
COPD Diagnosis
• Is indicative of airway inflammation and resistance.
coarse crackles (common)

• A common finding in exacerbations. A discontinuous sound referring to mucus or sputum in airways.
• Indicative of airway inflammation and mucus oversecretion.
tachypnea (uncommon)
• An increased respiratory rate occurs to compensate for hypoxia and hypoventilation.
• May involve use of accessory muscles.
asterixis (uncommon)
• Loss of postural control in outstretched arms (commonly known as a flap) caused by hypercapnia.
• This is due to impaired gas exchange in lung parenchyma, worsens with exercise, and is suggestive of
respiratory failure.
distended neck veins (uncommon)

• Occurs secondary to increased intrathoracic pressure and cor pulmonale.
lower-extremity swelling (uncommon)

• Suggests cor pulmonale and secondary pulmonary hypertension as a complication of advanced
chronic lung disease.
fatigue (uncommon)
• Occurs because of disrupted sleep secondary to constant nocturnal cough and persistent hypoxia and
hypercapnia.
headache (uncommon)
• May occur due to vasodilation caused by hypercapnia.
cyanosis (uncommon)
DIAGNOSIS
• Seen in the late stages of COPD, usually with hypoxia, hypercapnia, and cor pulmonale.
loud P2 (uncommon)
• Sign of advanced COPD.
• Indicates secondary pulmonary hypertension as a complication of cor pulmonale.
hepatojugular reflux (uncommon)

• Sign of advanced COPD complicated by cor pulmonale.
hepatosplenomegaly (uncommon)
• Sign of advanced COPD complicated by cor pulmonale.
clubbing (uncommon)
• COPD itself does not cause clubbing, but if tobacco exposure in COPD patients leads to lung cancer
and/or bronchiectasis, then clubbing may occur in COPD. Clubbing is usually not present until
significant impairment of lung function has occurred.
11
COPD Diagnosis
Diagnostic tests
1st test to order
Test Result
spirometry FEV1/FVC ratio <0.70; total
absence of reversibility
• COPD is classified based on the patient's FEV1 and its percentage
of the predicted FEV1. In cases where FVC may be hard to measure, is neither required nor the
most typical result
FEV6 (forced expiratory volume at 6 seconds) can be used.[18]
pulse oximetry low ox ygen saturation
• Checked as part of vital signs on acute presentation. A good pulse
wave should be picked up by the device. In patients with chronic
disease, an oxygen saturation of 88% to 90% may be acceptable.
• If <92% arterial or capillary blood gases should be checked.[1]
ABG PaCO₂ >50 mmHg and/
or PaO₂ of <60 mmHg
• Checked in patients who are acutely sick, especially if they have an
abnormal pulse oximetry reading. Should also be performed in stable suggests respiratory
insufficiency
patients with FEV1 <35% predicted or with clinical signs suggestive
of respiratory failure, or if peripheral arterial oxygen saturation is
<92%.
• Hypercapnia, hypoxia, and respiratory acidosis are signs of
impending respiratory failure and possible need for intubation.
CXR hyperinflation
• Seldom diagnostic, but useful in ruling out other pathologies.
• Increased anteroposterior ratio, flattened diaphragm, increased
intercostal spaces, and hyperlucent lungs may be seen.
[Fig-1]
[Fig-2]
• May also demonstrate complications of COPD, such as pneumonia
and pneumothorax.
DIAGNOSIS
CBC elevated hematocrit,

possible increased WBC
• This test may be considered to assess severity of an exacerbation
count
and may show polycythemia (hematocrit >55%), anemia, and
leukocytosis.[1]
ECG signs of right ventricular
• Risk factors for COPD are similar to those for ischemic heart disease, hypertrophy, arrhythmia,
ischemia
so comorbidity is common.
COPD Diagnosis
Other tests to consider
Test Result
pulmonary function tests obstructive pat tern,
decreased DLCO
• Useful for resolving diagnostic uncertainties and for preoperative
assessment.[1] Requires specialist laboratory facilities.
• Decreased diffusing capacity of the lung for carbon monoxide (DLCO)
is supportive of emphysema over chronic bronchitis.
chest CT scan hyperinflation
• Provides better visualization of type and distribution of lung tissue
damage and bulla formation than CXR.
[Fig-3]
• In contrast to smoking-related COPD, alpha-1 antitrypsin deficiency
mainly affects lower fields.
• Useful in excluding other underlying pulmonary disease and in
preoperative assessment.
sputum culture infecting organism
• In patients with frequent exacerbations, severe airflow limitation, and/
or exacerbations requiring mechanical ventilation, sputum should be
sent for culture.[1]
alpha-1 antitrypsin level should be normal in
patients with COPD
• Low level in patients with alpha-1 antitrypsin deficiency. Test is done
if there is high suspicion for alpha-1 antitrypsin deficiency, such as
a positive family history and atypical COPD cases (young patients
and nonsmokers). The World Health Organization recommends
that all patients with a diagnosis of COPD should be screened
once, especially in areas with high prevalence of alpha-1 antitrypsin
deficiency.[19]
exercise testing poor exercise
performance or exertional
• Can be of value in patients with a disproportional degree of dyspnea
hypoxemia is suggestive
compared with spirometry.[21] It can be performed on a cycle
DIAGNOSIS
of advanced disease
or treadmill ergometer, or by a simple timed walking test (e.g., 6
minutes, or duration <6 minutes).[22] Exercise testing is of use in
selecting patients for rehabilitation.
sleep study elevated apnea-hypopnea
• Obstructive sleep apnea, a common finding in patients with COPD, is index and/or nocturnal
associated with increased risk of death and hospitalization in patients hypoxemia
with COPD.[20]
respiratory muscle function reduced maximal
• Respiratory muscle function may be tested if dyspnea or hypercapnia inspiratory pressure
are disproportionately increased with respect to FEV1, as well
as in patients with poor nutrition and those with corticosteroid
myopathy.[23]
13
COPD Diagnosis
Differential diagnosis
Condition Differentiating signs / Differentiating tests

symptoms
Asthma • Onset of asthma is usually • Pulmonary function tests
in early life. A personal or (PFTs) show reversibility
family history of allergy, with bronchodilators and
rhinitis, and eczema is no decrease in diffusing
often present. There is daily capacity of the lung for
variability in symptoms, and carbon monoxide (DLCO).
patients have overt wheezing Sputum or blood eosinophilia
that usually rapidly responds is suggestive of asthma.
to bronchodilators. Cough
variant asthma mimics many
features of COPD.
Congestive heart failure • Usually a history of • B-type natriuretic peptide

cardiovascular diseases levels are usually elevated,
is present. Patients report and CXR reveals increased
symptoms of orthopnea, pulmonary vascular
and fine bibasilar inspiratory congestion. Echocardiogram
crackles may be heard on may confirm the diagnosis.
auscultation.
Bronchiectasis • There may be a history • Chest CT reveals bronchial

of recurrent infection in dilation and bronchial wall
childhood. Large volume thickening.
of purulent sputum is
usually present. Coarse
crackles may be heard on
auscultation. History of
pertussis or tuberculosis is a
clue to diagnosis.
DIAGNOSIS
Tuberculosis • A history of fever, night • The diagnosis requires

sweats, weight loss, and microbiologic confirmation.
chronic productive cough is Infiltrates, fibrosis, or
usually present. Tuberculosis granuloma seen on CXR
is more common in people or chest CT may suggest
living in or originating from tuberculosis. Patients usually
endemic areas. have positive skin test for
tuberculosis.
Bronchiolitis • Bronchiolitis may affect • PFTs in bronchiolitis can

patients at younger ages. present with obstructive,
The patient may have restrictive, or mixed pattern.
a history of connective CXR shows hyperinflation.
tissue disorders, especially High-resolution chest
rheumatoid arthritis, or fume CT may show diffuse,
exposure. Some cases are small, centrilobular nodular
postinfectious. opacities, but is rarely done
in children due to radiation
risk.
Upper airway dysfunction • Can affect patients of any • The flow-volume curve in
age. History of prior trauma pulmonary function testing
COPD Diagnosis
Condition Differentiating signs / Differentiating tests

symptoms
or intubation is very helpful. may reveal a characteristic
Lung examination is usually expiratory or inspiratory
normal, but signs of upper plateau, or both. Diagnosis
airway restriction, such as is confirmed by direct
wheezing and stridor, may visualization of the affected
be present. Patients may airway by endoscopy.
have voice hoarseness if
vocal cords are involved.
Chronic sinusitis/ • Chronic sinusitis/rhinitis is • CT of sinuses and/or empiric

postnasal drip a very common cause of trial of antihistamines are
chronic cough. Patients may commonly utilized to aid in
complain of sinus pressure, diagnosis.
rhinorrhea, nonproductive
cough, and/or headache.
Gastroesophageal reflux • Patients with GERD often • Diagnosis is usually based

disease (GERD) have dyspepsia and frequent on response to empiric
belching, and can have a therapy with proton-pump
chronic cough that worsens inhibitors.
at night when supine.
ACE inhibitor-induced • ACE inhibitors can cause • Diagnosis is usually

chronic cough chronic cough; however, based on improvement of
the cough is usually symptoms after empiric
nonproductive. cessation of ACE inhibitor.
Lung cancer • Patients may have weight • Radiography is important

loss, night sweats, in the assessment for lung
hemoptysis, and/or chest or cancer. Bronchoscopy may
back pain. be necessary to evaluate
• People with COPD are also for endobronchial cancer if
at increased risk of lung suspicion is high.
cancer.
DIAGNOSIS
Diagnostic criteria
Global Initiative for Chronic Obstructive Lung Disease (GOLD)
criteria[1]
Classification of severity of airflow limitation in COPD:
In pulmonary function testing, a postbronchodilator FEV1/FVC ratio of <0.70 is commonly considered

diagnostic for COPD. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) system categorizes
airflow limitation into stages. In patients with FEV1/FVC <0.70:
• GOLD 1 - mild: FEV1≥ 80% predicted

• GOLD 2 - moderate: 50% ≤FEV1 <80% predicted
• GOLD 3 - severe: 30% ≤FEV1 <50% predicted
• GOLD 4 - very severe: FEV1 <30% predicted.
15
COPD Diagnosis
The GOLD guideline uses a combined COPD assessment approach to group patients according to
symptoms and previous history of exacerbations. Symptoms are assessed using the Modified British Medical
Research Council (mMRC) or COPD assessment test (CAT) scale. These can be found in the GOLD
guidelines.[1]
• Group A: low risk (0-1 exacerbation per year, not requiring hospitalization) and fewer symptoms
(mMRC 0-1 or CAT <10)
• Group B: low risk (0-1 exacerbation per year, not requiring hospitalization) and more symptoms
(mMRC≥ 2 or CAT≥ 10)
• Group C: high risk (≥2 exacerbations per year, or one or more requiring hospitalization) and fewer
symptoms (mMRC 0-1 or CAT <10)
• Group D: high risk (≥2 exacerbations per year, or one or more requiring hospitalization) and more
symptoms (mMRC≥ 2 or CAT≥ 10).
DIAGNOSIS
COPD Treatment
Step-by-step treatment approach

The ultimate goals of treatment of COPD are to prevent and control symptoms, to reduce the severity and
number of exacerbations, to improve respiratory capacity for increased exercise tolerance, and to reduce
mortality.[27] There is a stepwise approach to therapy, but it is important to remember that treatment should
be individualized for general health status and comorbid conditions.
The therapeutic approach involves reducing risk factor exposure, appropriate assessment of disease,
patient education, pharmacologic and nonpharmacologic management of stable COPD, and prevention and
treatment of acute COPD exacerbations.
Continuous assessment and monitoring of disease

Ongoing monitoring and assessment in COPD ensures that the goals of treatment are being met.
Quality of life and patients' sense of wellbeing will improve, and hospital admissions will be significantly
decreased in cases where self- or professional monitoring of disease is being utilized.[28] Such
assessment of the medical history should include:
Exposure to risk factors and preventive measures:
• Tobacco smoke
• Occupational exposures (fumes, dust, etc.)
• Influenza and pneumococcal vaccination.
Disease progression and development of complications:
• Decline in exercise tolerance

• Increased symptoms
• Worsened sleep quality
• Missed work or other activities.
Pharmacotherapy and other medical treatment:
• How often rescue inhaler is used

• Any new medicines
• Compliance with medical regimen
• Ability to use inhalers properly
• Adverse effects.
Exacerbation history:
• Urgent care or emergency room visits

• Recent oral corticosteroid bursts
• Frequency, severity, and likely causes of exacerbations should be evaluated.
Comorbidities:
TREATMENT
• Assessment of coexisting medical problems (e.g., heart failure).

In addition, objective assessment of lung function should be obtained yearly or more frequently if there is
a substantial increase in symptoms.
17
COPD Treatment
Integrated disease management (IDM) in which several healthcare providers (physical therapist,
pulmonologist, nurse, etc.) worked together with patients has been shown to improve quality of life and
decrease hospital admissions.[29]
Acute exacerbations
An exacerbation of COPD is defined as an event characterized by a change in the patient's baseline
dyspnea, cough, and/or sputum that is beyond normal day-to-day variations and is acute in onset. See our
topic on Acute exacerbation of chronic obstructive pulmonary disease for further information.
Chronic management: stepwise therapy according to Global

Initiative for Chronic Obstructive Lung Disease (GOLD) class
GOLD guidelines[27] recommend a stepwise approach to pharmacologic therapy:
• For group A patients (few symptoms and low risk of exacerbations), a bronchodilator is offered
first-line. This can be either a short- or a long-acting bronchodilator. This should be continued if
symptomatic benefit is documented.
• For group B patients (more symptoms and low risk of exacerbations), a long-acting bronchodilator
should be offered first-line. If the patient has persistent symptoms when taking one long-acting
bronchodilator, then the use of two bronchodilators is recommended. For patients with severe
breathlessness, initial treatment with two bronchodilators may be warranted.1[A]Evidence
• For group C patients (few symptoms but higher risk of exacerbations), first-line treatment should be
a long-acting bronchodilator, and GOLD recommends starting a long-acting muscarinic antagonist
(LAMA) in this group. Patients who experience further exacerbations may benefit from adding
a second long-acting bronchodilator (long-acting beta-2-agonist [LABA] or LAMA) or using a
combination of a LABA and an inhaled corticosteroid (ICS). GOLD recommends a LABA/LAMA
combination over LABA/ICS, as ICS increases the risk of developing pneumonia in some patients.
• For group D patients (more symptoms and high risk of exacerbations), GOLD recommends starting
therapy with a LABA/LAMA combination. If patients experience further exacerbations when on
LABA/LAMA, they can either try escalation to LABA/LAMA/ICS, or they can switch to LABA/ICS.
If patients treated with LABA/LAMA/ICS still have exacerbations, then additional options include
adding roflumilast, or a macrolide, or stopping the ICS.
All patients are candidates for education, vaccination, and smoking cessation interventions.2[A]Evidence
Bronchodilator therapy options

Beta agonists are widely used in the treatment of COPD.3[A]Evidence They increase intracellular cAMP,
leading to respiratory smooth muscle relaxation and reduced airway resistance. They are available
as short-acting and long-acting preparations. Short-acting beta-2 agonists improve lung function and
breathlessness and quality of life. These agents can be used as rescue therapy when the patient is using
long-acting beta-2 agonist therapy.[30] LABAs improve lung function, breathlessness, exacerbation rate,
and number of hospitalizations, but do not affect mortality or rate of decline of lung function.[27]
A muscarinic antagonist is a type of anticholinergic agent that acts as a bronchodilator by blocking the
TREATMENT
cholinergic receptors on the respiratory smooth muscle. This causes muscle relaxation and reduces
airflow limitation.4[B]Evidence Inhaled muscarinic antagonists are available as both short- and long-acting
preparations. Tiotropium, a LAMA, has been shown to reduce risk of exacerbation versus placebo or
other maintenance treatments.[31] Newer LAMAs, such as aclidinium, glycopyrrolate, and umeclidinium,
have at least comparable efficacy to tiotropium, in terms of change from baseline in trough forced
COPD Treatment
expiratory volume in 1 second (FEV1), transitional dyspnea index focal score, St George's Respiratory
Questionnaire score, and rescue medication use.[32] There is a suggestion of increased cardiovascular-
related mortality in some studies of patients taking short-acting muscarinic antagonists and in some
studies of patients taking LAMAs.[33] [34] A population-based cohort study found that older men with
COPD newly started on LAMAs are at increased risk of urinary tract infections.[35]
Beta agonists and muscarinic antagonists, therefore, provide bronchodilator effects through different
pathways. Their combination may provide a better therapeutic effect without increasing the adverse
effects of each class.[36] [37] [38] [39] 1[A]Evidence Compared to LABA/ICS, a LABA/LAMA combination
has fewer exacerbations, a larger improvement of FEV1, a lower risk of pneumonia, and more frequent
improvement in quality of life.[40] A systematic review and network meta-analysis found that all LABA/
LAMA fixed-dose combinations had a similar efficacy and safety.[41]
In cases of stable COPD, if the decision is made to use single-agent therapy, LAMA may be superior
to LABA agents.[36] Clinical trials have shown that LAMA have a greater effect on reducing rates of
exacerbations compared with LABA.[42] [43] The long-term safety of LAMA was demonstrated in the
UPLIFT trial.[44] As outlined above, GOLD makes recommendations on the initial agent based on the
patient’s risk group (A, B, C, or D).[27]
Theophylline (a methylxanthine agent) is a bronchodilator that acts by increasing cAMP and subsequent
respiratory smooth muscle relaxation. It is not commonly used because of limited potency, narrow
therapeutic window, high-risk profile, and frequent drug-drug interactions. Theophylline is indicated
for persistent symptoms if inhaled therapy is insufficient to relieve airflow obstruction.5[A]Evidence
Theophylline has modest effects on lung function in moderate to severe COPD.[45]
Umeclidinium/vilanterol is a LABA/LAMA approved for use in COPD.[46] Glycopyrrolate/formoterol

fumarate is another LABA/LAMA combination approved for COPD patients,[47] as is indacaterol/
glycopyrrolate.[48] [49] This once-daily inhaler showed superior efficacy compared with glycopyrrolate
plus tiotropium in patients with moderate to severe COPD,[50] and compared with salmeterol/fluticasone
in preventing COPD exacerbation.[51]
Inhaled corticosteroids
Inhaled corticosteroids are indicated in patients with advanced stages of COPD who suffer from frequent
exacerbations.[52] They should be added to the patient's existing bronchodilator therapy and should
not be used as monotherapy.[27] Inhaled corticosteroids are believed to be effective because of their
anti-inflammatory effects. Long-term inhaled corticosteroid use reduces the need to use rescue therapy
and reduces exacerbations, and may also decrease mortality.[53] [54] Several studies have pointed to
an increased risk of pneumonia in COPD patients taking inhaled corticosteroids.[55] This risk is slightly
higher for fluticasone in comparison with budesonide.[56] A systematic review and meta-analysis found
that, despite a significant increase in unadjusted risk of pneumonia associated with use of inhaled
corticosteroids, pneumonia fatality and overall mortality were not increased in randomized controlled
trials and were decreased in observational studies.[57] Therefore, an individualized treatment approach
that assesses a patient's risk of pneumonia versus the benefit of decreased exacerbations should be
implemented.[55] [58] [59] Concern is also raised with regards to increased risk of tuberculosis and
TREATMENT
influenza in adult patients with COPD who are on inhaled corticosteroid therapy.[60]
According to the GOLD guideline, inhaled corticosteroids are not recommended as first-line therapy in
any of the patient groups A to D. They are only recommended as part of escalation of therapy if patients
continue to experience exacerbations despite taking a long-acting bronchodilator.[27]
19
COPD Treatment
Phosphodiesterase-4 inhibitors
Roflumilast is an oral phosphodiesterase-4 inhibitor that may reduce exacerbations in group D patients at
risk for frequent exacerbations when not adequately controlled by long-acting bronchodilators.[27] This
agent offers benefit in improving lung function and reducing the likelihood of exacerbations. However, it
has little impact on quality of life or symptoms.[61]
Combined bronchodilator and corticosteroid preparations

A combination preparation of long-acting bronchodilator and inhaled corticosteroid may be used for
patients who require both these agents. This is convenient and may help with compliance in some
patients. The choice of therapy in this class is based on availability and individual response and
preference.[62] Combination therapy with inhaled corticosteroid and a long-acting beta agonist is
superior to use of either agent alone.[63] [64] The combination may be provided in separate inhalers or a
combination inhaler.
Multiple studies support triple therapy with LABA/LAMA/ICS as being superior to single- or double-agent
therapy with LABA/LAMA or LABA/ICS regarding rate of moderate to severe COPD exacerbations[65]
[66] [67] [68] and rate of hospitalization.[69] [70]
Patient education and self-management

All patients should be well educated about the disease course and symptoms of exacerbation or
decompensation. Their expectation of the disease, treatment, and prognosis should be realistic. It is
important to remember that no medication has been shown to modify the long-term decline in lung
function, and the primary goal of pharmacotherapy is to control symptoms and prevent complications.
One Cochrane review found that self-management interventions that include an action plan for acute
exacerbations of COPD are associated with improvements in health-related quality of life and fewer
admissions to the hospital for respiratory problems. An exploratory analysis found a small, but significantly
higher, respiratory-related mortality rate for self-management compared to usual care, although no excess
risk of all-cause mortality was seen.[71]
One randomized controlled trial found that a telephone health coaching intervention to promote behavior
change in patients with mild COPD in primary care led to improvements in self-management activities, but
did not improve health-related quality of life.[72]
Physical activity is recommended for all patients with COPD.[27] One systematic review and meta-
analysis of randomized controlled trials found that exercise training on its own can improve physical
activity in COPD, and greater improvements can be made with the addition of physical activity
counseling.[73] Another systematic review and meta-analysis found that a combination of aerobic
exercise and strength training was more effective than strength training or endurance training alone in
increasing the 6-minute walking distance.[74]
Smoking cessation and vaccination

Smoking cessation should be encouraged in all patients, in addition to guidance on avoiding occupational
TREATMENT
or environmental tobacco smoke exposures.
Usual smoking cessation programs include counseling, group meetings, and drug therapy.[75] Some
patients may need frequent referrals to achieve success. Smoking cessation significantly reduces the
rate of progression of COPD and risk of malignancies.2[A]Evidence It also reduces risk of coronary and
COPD Treatment
cerebrovascular diseases. Smoking cessation that includes pharmacotherapy and intensive counseling
has a higher success rate and is cost effective in COPD, with low costs per quality-adjusted life year.[76]
[77] [78]
Patients should be vaccinated against influenza virus and Streptococcus pneumoniae .[27] [79]
Vaccination against influenza is associated with fewer exacerbations of COPD.[79] [80]
Mucolytics
Patients with the chronic bronchitis phenotype of COPD often produce thick sputum on a frequent basis.
Mucolytic agents are not associated with an increase in adverse effects and may be beneficial during
exacerbations of COPD. They result in a small reduction in the frequency of acute exacerbations, but
do not improve lung function or quality of life. Mucolytic agents may be most beneficial for patients not
on inhaled corticosteroids.[81] The use of positive expiratory pressure (PEP) therapy to clear secretions
during acute exacerbations has been found to improve subjective feelings of breathlessness but was not
associated with decreased hospitalizations or rate of exacerbations.[82]
Pulmonary rehabilitation
Pulmonary rehabilitation should be initiated for patients who remain symptomatic despite bronchodilator
therapy and is recommended to start early in the course of the disease, when they start feeling shortness
of breath with regular activity and walking on a level surface. Its effect is beneficial in improving exercise
capacity and quality of life. It also decreases the depression and anxiety related to this disease, and
reduces hospitalization in COPD patients.[83] The benefit appears to subside after termination of the
course unless patients follow a home exercise schedule.[84] Benefits of home- or community-based
pulmonary rehabilitation on respiratory symptoms and quality of life in patients with COPD could match
those of the hospital-based rehabilitation programs.[85] [86] Although pulmonary rehabilitation relieves
dyspnea and fatigue, improves emotional function, and enhances a sense of control to a moderately
large and clinically significant extent,[87] it is important to remember that early progressive exercise
rehabilitation beyond current standard physical therapy practice during hospital admission for COPD is not
recommended and could be associated with a higher 12-month mortality.[88] There is evidence to support
starting pulmonary rehabilitation within 1 month of an acute exacerbation.[89] [90]
GOLD guidelines recommend pulmonary rehabilitation for patient groups B to D.[27]
Ox ygen therapy
GOLD guidelines recommend long-term oxygen therapy in stable patients who have:[27]
• PaO₂ ≤7.3 kPa (55 mmHg) or SaO₂ ≤88%, with or without hypercapnia confirmed twice over a 3-
week period; or
• PaO₂ between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg), or SaO₂ of 88%, if there is evidence of
pulmonary hypertension, peripheral edema suggesting congestive cardiac failure, or polycythemia
(hematocrit > 55%).
Oxygen therapy helps minimize pulmonary hypertension by decreasing pulmonary artery pressure,
TREATMENT
and improves exercise tolerance and quality of life. It has been shown to improve survival.[27] [91] [92]
6[B]Evidence
21
COPD Treatment
Oxygen is suggested for patients in whom the predicted PaO₂ during air travel is <6.7 kPa (<50
mmHg).[27] These patients usually have a saturation of <92% in room air at sea level. If in doubt, patients
could undergo testing to be evaluated for their predicted PaO₂ during flight.
There is some evidence that oxygen can relieve breathlessness when given during exercise to mildly
hypoxemic and nonhypoxemic people with COPD who do not otherwise qualify for home oxygen
therapy.[93]
Surgery
Surgical interventions (bullectomy, lung volume reduction surgery,[94] [95] and lung transplant) are the
last step in the management of COPD. They are used to improve lung dynamics, exercise adherence,
and quality of life.[96] Endobronchial valve insertion can produce clinically meaningful improvements in
appropriately selected COPD patients.[97]
Criteria for referral for lung transplantation include:[98]
• Progressive disease, despite maximal treatment including medication, pulmonary rehabilitation,

and oxygen therapy.
• Patient is not a candidate for endoscopic or surgical lung volume reduction surgery (LVRS).
Simultaneous referral of patients with COPD for both lung transplant and LVRS evaluation is
appropriate.
• Body mass index, airflow Obstruction, Dyspnea, and Exercise (BODE) index of 5 to 6.
• PaCO₂ >50 mmHg or 6.6 kPa and/or PaO₂ <60 mmHg or 8 kPa.
• FEV1 <25% predicted.
[VIDEO: BODE Index for COPD Survival Prediction ]
Palliative care
For some patients with very advanced end-stage COPD, palliative care and hospice admission should
be considered. Patient and family should be well educated about the process, and it is suggested
that discussions should be held early in the course of the disease before acute respiratory failure
develops.[99] One study has suggested that low doses of an opioid analgesic and a benzodiazepine are
safe and are not associated with increased hospital admissions or mortality.[100]
One Cochrane review concluded that there is no evidence for or against benzodiazepines for the relief of
breathlessness in people with advanced cancer and COPD.[101]
Treatment details overview

Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
TREATMENT
COPD Treatment
Acute ( summary )
group A: few symptoms and low risk
of exacerbations
1st short- or long-acting bronchodilator
plus patient education and vaccination
plus smoking cessation
group B: more symptoms and low

risk of exacerbations
1st long-acting bronchodilator
plus short-acting bronchodilator as required
plus pulmonary rehabilitation
adjunct long-term ox ygen therapy
2nd dual long-acting bronchodilator therapy
group C: few symptoms but higher

adjunct theophylline

TREATMENT
23
COPD Treatment
Acute ( summary )
3rd long-acting beta-2 agonist plus inhaled

corticosteroid
group D: more symptoms and high

1st dual long-acting bronchodilator therapy
adjunct surgical interventions
adjunct palliative care
2nd triple therapy: long-acting beta-2 agonist

(LABA) plus long-acting muscarinic
antagonist (LAMA) plus inhaled
corticosteroid (ICS)
adjunct phosphodiesterase-4 inhibitor

TREATMENT
adjunct macrolide antibiotic
COPD Treatment
Acute ( summary )
2nd long-acting beta-2 agonist (LABA) plus

inhaled corticosteroid (ICS)
TREATMENT
25
COPD Treatment
Treatment options
Please note that formulations/routes and doses may differ between drug names and brands, drug
formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer
TREATMENT
COPD Treatment
Acute
group A: few symptoms and low risk
of exacerbations
1st short- or long-acting bronchodilator

Primary options
» albuterol inhaled: (90 micrograms/dose

inhaler) 90-180 micrograms (1-2 puffs) every
4-6 hours when required
OR
» levalbuterol inhaled: (45 micrograms/dose

OR
» ipratropium bromide inhaled: (17

micrograms/dose inhaler) 34 micrograms (2
puffs) up to four times a day when required,
maximum 204 micrograms/day
OR
» salmeterol inhaled: (50 micrograms/dose

inhaler) 50 micrograms (1 puff) twice daily
OR
» indacaterol inhaled: (75 microgram/capsule

inhaler) 75 micrograms (1 capsule) once daily
OR
» arformoterol inhaled: 15 micrograms

nebulized twice daily
OR
» olodaterol inhaled: (2.5 micrograms/dose

inhaler) 5 micrograms (2 sprays) once daily
OR
» tiotropium inhaled: (18 micrograms/capsule

inhaler) 18 micrograms (1 capsule) once
daily; (2.5 micrograms/dose inhaler) 5
TREATMENT
micrograms (2 sprays) once daily
OR
27
COPD Treatment
Acute
» umeclidinium inhaled: (62.5 micrograms/
dose inhaler) 62.5 micrograms (1 puff) once
daily
OR
» aclidinium bromide inhaled: (400

puff) twice daily
OR
» glycopyrrolate inhaled: (15.6 micrograms/

capsule inhaler) 15.6 micrograms (1 capsule)
twice daily; (25 micrograms/vial nebulizer
inhalation solution) 25 micrograms nebulized
twice daily using Magnair® nebulizer device
» Global Initiative for Chronic Obstructive Lung

Disease (GOLD) guidelines state that all group
A patients should be offered bronchodilator
treatment based on its effect on breathlessness.
This can be either a short- or a long-acting
bronchodilator.[27]
» The effect of the bronchodilator should be

evaluated. Depending on the response, it should
be continued or stopped or another class of
bronchodilator should be tried.[27]
» Short-acting bronchodilators provide

symptomatic relief.7[A]Evidence
» Failure to respond to short-acting

bronchodilator may signify an acute
exacerbation.
» Patients should not take short-acting

anticholinergic agents if they have already been
started on tiotropium.[102] [103]
» Short-acting drugs include albuterol,

levalbuterol, and ipratropium.
» Long-acting drugs include salmeterol,

indacaterol, arformoterol, olodaterol, tiotropium,
umeclidinium, aclidinium, and glycopyrrolate.
Treatment recommended for ALL patients in
selected patient group
TREATMENT
» Influenza and pneumococcal vaccination

should be offered to every COPD patient.[27]
Influenza vaccine is given annually.
Pneumococcal vaccine should be given to
COPD patients older than 65 years of age and
to younger patients with significant comorbid
COPD Treatment
Acute
conditions. This vaccine also reduces incidence
of community-acquired pneumonia in patients
younger than 65 with an FEV1 of <40%.[104]
» Patients should be well educated about the

disease course and symptoms of exacerbation
or decompensation. Physical activity is
recommended for all patients with COPD.[27]
» Discussions should be held early in the course

of the disease, before acute respiratory failure
develops, about the possible need for and
benefits of palliative care in the future.[99]
» All patients should be strongly recommended
not to start smoking, or to stop if they are current
smokers. Smoking cessation is a primary goal in
management of COPD.2[A]Evidence
» Nicotine-replacement therapy or other drug

therapies, in conjunction with appropriate
nonpharmacologic therapies, should be used.
group B: more symptoms and low risk
of exacerbations

Primary options
» salmeterol inhaled: (50 micrograms/dose

inhaler) 50 micrograms (1 puff) twice daily
OR
» indacaterol inhaled: (75 microgram/capsule

inhaler) 75 micrograms (1 capsule) once daily
OR
» arformoterol inhaled: 15 micrograms

nebulized twice daily
OR
» olodaterol inhaled: (2.5 micrograms/dose

inhaler) 5 micrograms (2 sprays) once daily
TREATMENT
OR

29
COPD Treatment
Acute
OR

daily
OR

puff) twice daily
OR

» Long-acting muscarinic antagonists (LAMA)

or long-acting beta-2 agonists (LABA)[105] can
be used as first-line therapy in this group of
patients.[27]
» According to Global Initiative for Chronic

Obstructive Lung Disease (GOLD) guidelines,
long-acting inhaled bronchodilators are superior
to short-acting bronchodilators when taken as
needed and are, therefore, recommended in this
patient group.[27] [106] [107]
» According to GOLD guidelines, there is no

evidence to recommend one class of long-acting
bronchodilator over another for initial relief of
symptoms in this group of patients. The choice
should depend on the patient's perception of
symptom relief.[27]
» For patients with severe breathlessness,

initial therapy with two bronchodilators may be
considered.[27]
» For patients with persistent breathlessness on

monotherapy, GOLD guidelines recommend the
use of two bronchodilators.[27]

TREATMENT

Primary options
COPD Treatment
Acute
OR

OR

» Provides symptomatic relief.7[A]Evidence

exacerbation.



TREATMENT

31
COPD Treatment
Acute

» Pulmonary rehabilitation should be started
early.[27]
» The principal goals of pulmonary rehabilitation

are to reduce symptoms, improve quality of
life, and increase physical and emotional
participation in everyday activities. Pulmonary
rehabilitation can result in significant and
clinically meaningful improvements in
multiple outcome areas, including dyspnea,
exercise ability, health status, and healthcare
utilization.[27] [91]
Treatment recommended for SOME patients in
» Criteria for long-term oxygen therapy include:
PaO₂ ≤7.3 kPa (55 mmHg); or SaO₂ ≤88%,
with or without hypercapnia confirmed twice
over a 3-week period; or PaO₂ between 7.3
kPa (55 mmHg) and 8.0 kPa (60 mmHg), or
SaO₂ of 88%, if there is evidence of pulmonary
hypertension, peripheral edema suggesting
congestive cardiac failure, or polycythemia
(hematocrit >55%).[27]
» Oxygen is suggested for patients in whom

the predicted PaO₂ during air travel is <6.7 kPa
(<50 mmHg).[27] These patients usually have
a saturation of <92% in room air at sea level. If
in doubt, patients could undergo testing to be
evaluated for their predicted PaO₂ during flight.
» The therapeutic goal is to increase the

PaO₂ to at least 5 mmHg above the patient's
baseline value and to a minimum of 60 mmHg.
In addition, oxygen saturation should stay above
90% during rest, exercise, and sleep.[91] [96]
6[B]Evidence
TREATMENT
Primary options
» umeclidinium/vilanterol inhaled: (62.5/25

micrograms/dose inhaler) 1 puff once daily
OR
COPD Treatment
Acute
» glycopyrrolate/formoterol fumarate inhaled:

(9/4.8 micrograms/dose inhaler) 2 puffs twice
daily
OR
» indacaterol/glycopyrrolate inhaled:
(27.5/15.6 micrograms/capsule inhaler) 1
capsule twice daily
OR
» tiotropium/olodaterol inhaled: (2.5/2.5

micrograms/dose inhaler) 2 puffs once daily
» For patients with persistent breathlessness

on monotherapy, Global Initiative for Chronic
Obstructive Lung Disease (GOLD) guidelines
recommend the use of two bronchodilators.[27]
» If two bronchodilators do not improve

symptoms, GOLD guidelines suggest stepping
down again to a single bronchodilator.[27]
» Umeclidinium/vilanterol, glycopyrrolate/
formoterol fumarate,[47] indacaterol/
glycopyrrolate,[51] and tiotropium/olodaterol are
combinations of a long-acting beta-2 agonist
(LABA) and a long-acting muscarinic antagonist
(LAMA) approved for use in COPD.[46]
Primary options

OR

OR
TREATMENT

33
COPD Treatment
Acute
exacerbation.




early.[27]

TREATMENT

rehabilitation can result in significant and
clinically meaningful improvements in
COPD Treatment
Acute
exercise ability, health status, and healthcare
utilization.[27] [91]


6[B]Evidence
group C: few symptoms but higher

Primary options

OR

daily
OR

TREATMENT

puff) twice daily
OR
35
COPD Treatment
Acute
» Initial treatment in group C should be a single

long-acting bronchodilator.[27] In two head-
to-head comparisons, the tested long-acting
muscarinic antagonist (LAMA) was better
than the long-acting beta-2 agonist (LABA) at
preventing exacerbations.[42] [43] Therefore,
Global Initiative for Chronic Obstructive Lung
Disease (GOLD) guidelines recommend starting
with a LAMA in patient group C.

Primary options

OR

OR


exacerbation.

TREATMENT

COPD Treatment
Acute



early.[27]

rehabilitation can result in improvements in
exercise, quality of life, and emotional
feelings.[27] [91]
TREATMENT
Primary options
» theophylline: 300 mg/day orally (immediate-

release) initially given in divided doses every
6-8 hours, increase to 400 mg/day after 3
days, then 600 mg/day after another 3 days;
37
COPD Treatment
Acute
adjust dose according to serum drug level
and response
» There is no clear recommendation about the

exactly appropriate time to use theophylline,
but most experts believe in its use when
patients have exhausted bronchodilator and
corticosteroid options.
» Toxicity is dose-related.5[A]Evidence


6[B]Evidence
Primary options

OR

daily
OR
TREATMENT
capsule twice daily
OR
COPD Treatment
Acute

» Patients in group C with persistent

exacerbations may benefit from dual therapy with
a long-acting beta-2 agonist (LABA) and a long-
acting muscarinic antagonist (LAMA).[27]
combinations of a LABA and a LAMA approved
for use in COPD.[46]
Primary options

OR

OR


exacerbation.

TREATMENT

39
COPD Treatment
Acute



early.[27]

exercise, quality of life, and emotional
feelings.[27] [91]
Primary options

TREATMENT

and response

COPD Treatment
Acute


6[B]Evidence
3rd long-acting beta-2 agonist plus inhaled
corticosteroid
Primary options
» fluticasone furoate/vilanterol inhaled:

(100/25 micrograms/dose inhaler) 1 puff once
daily
OR
» fluticasone propionate/salmeterol inhaled:

(250/50 micrograms/dose inhaler) 1 puff
twice daily
OR
» budesonide/formoterol inhaled: (160/4.5

TREATMENT
micrograms/dose inhaler) 2 puffs twice daily
OR
41
COPD Treatment
Acute
» mometasone/formoterol inhaled: (100/5
micrograms/dose inhaler; 200/5 micrograms/
dose inhaler) 2 puffs twice daily
» Patients with persistent exacerbations may

benefit from using a combination of a long-
acting beta-2 agonist (LABA) and an inhaled
corticosteroid (ICS). As inhaled corticosteroids
increase the risk of developing pneumonia in
some patients, the Global Initiative for Chronic
prefer dual long-acting bronchodilator therapy
over a LABA/ICS combination.[27]
» A combination preparation of a LABA and an

ICS may be used for patients who require both
these agents. This is convenient and may help
with compliance in some patients. The choice of
therapy in this class is based on availability and
individual response and preference. Combination
therapy with a LABA and an ICS is superior
to use of either agent alone. The combination
may be provided in separate inhalers or a
combination inhaler (combination formulations
are detailed here).
Primary options

OR

OR


TREATMENT

exacerbation.

COPD Treatment
Acute



early.[27]

exercise capacity, quality of life, and emotional
feelings.[27] [91]
TREATMENT
Primary options
43
COPD Treatment
Acute
and response



6[B]Evidence
group D: more symptoms and high
1st dual long-acting bronchodilator therapy

Primary options

TREATMENT
OR

daily
COPD Treatment
Acute
OR
capsule twice daily
OR

» The Global Initiative for Chronic Obstructive

Lung Disease (GOLD) guidelines recommend
starting treatment with a long-acting beta-2
agonist (LABA) and long-acting muscarinic
antagonist (LAMA) combination in group D.
This is because the LABA/LAMA combinations
showed superior results compared to the single
drugs in studies with patient reported outcomes
as the primary endpoint.[27]
» In addition, a LABA/LAMA combination was

superior to a LABA and an inhaled corticosteroid
(ICS) combination in preventing exacerbations
and other patient reported outcomes in group D
patients.[27]
» Group D patients are at a higher risk of

developing pneumonia when receiving treatment
with ICS.[42] [108]
» If a single bronchodilator is chosen as initial

treatment, a LAMA is preferred by GOLD
guidelines over a LABA.[27]
» In some patients, initial treatment with LABA/

ICS combination may be the first choice. These
patients may have a history and/or findings
suggestive of asthma-COPD overlap.[27]

combinations of a LABA and a LAMA approved
for use in COPD.[46]
TREATMENT

Primary options
45
COPD Treatment
Acute
OR

OR


exacerbation.


TREATMENT


COPD Treatment
Acute
» Pulmonary rehabilitation should be started as
early as patient group B or C disease.[27]

feelings.[27] [91]
Primary options

and response


TREATMENT

47
COPD Treatment
Acute
6[B]Evidence
» Criteria for referral for lung transplantation
include: progressive disease, despite maximal
treatment including medication, pulmonary
rehabilitation, and oxygen therapy; patient is
not a candidate for endoscopic or surgical lung
volume reduction surgery (LVRS) (simultaneous
referral of patients with COPD for both lung
transplant and LVRS evaluation is appropriate);
Body mass index, airflow Obstruction, Dyspnea,
and Exercise (BODE) index of 5 to 6; PaCO₂ >50
mmHg or 6.6 kPa and/or PaO₂ <60 mmHg or 8
kPa; FEV1 <25% predicted.[98]
» LVRS is indicated in patients with very severe

airflow limitation and especially in patients with
localized upper lobe disease and lower than
normal exercise capacity.[94] Bullectomy is an
option in COPD patients with dyspnea in whom
CT reveals huge bullae occupying at least 30%
of the hemithorax. Severely poor functional
status and severe decrease in FEV1 (<500 mL)
make these options less favorable.
» Lung transplantation has been shown

to improve quality of life and functional
capacity.[109] [110] However, lung
transplantation does not appear to confer a
survival benefit.[111]
[VIDEO: BODE Index for COPD

Survival Prediction ]
» For some patients with very advanced end-
stage COPD, palliative care and hospice
admission should be considered. Patient and
TREATMENT
family should be well educated about the

process, and it is suggested that discussions
should be held early in the course of the disease
before acute respiratory failure develops.[99]
One study has suggested that low doses of an
opioid analgesic and a benzodiazepine are safe
COPD Treatment
Acute
and are not associated with increased hospital
admissions or mortality.[100] One Cochrane
review concluded that there is no evidence
for or against benzodiazepines for the relief of
breathlessness in people with advanced cancer
and COPD.[101]
2nd triple therapy: long-acting beta-2 agonist
(LABA) plus long-acting muscarinic
antagonist (LAMA) plus inhaled
corticosteroid (ICS)
Primary options
» fluticasone furoate/umeclidinium/vilanterol
inhaled: (100/62.5/25 micrograms/dose
inhaler) 1 puff once daily
OR

daily
-or-
twice daily
-or-
-or-
--AND--
-or-
daily
-or-
puff) twice daily
-or-
TREATMENT

» In group D patients who develop further

exacerbations on LABA/LAMA therapy, the
Global Initiative for Chronic Obstructive Lung
49
COPD Treatment
Acute
Disease (GOLD) guidelines suggest two
alternative pathways: escalation to LABA/LAMA/
ICS or switch to LABA/ICS.[27]
» Multiple studies support triple therapy with

LABA/LAMA/ICS as being superior to single-
or double-agent therapy with LABA/LAMA or
LABA/ICS regarding rate of moderate to severe
COPD exacerbations[65] [66] [67] [68] and rate
of hospitalization.[69] [70]
» If patients treated with LABA/LAMA/ICS (triple

therapy) still have exacerbations, additional
options include adding roflumilast, adding a
macrolide antibiotic, and stopping the ICS.[27]
Stopping the ICS may be appropriate if a lack of
efficacy is reported, if there is an elevated risk of
adverse events (including pneumonia), or if there
would be no significant harm from withdrawal of
ICS.[27]
Primary options

OR

OR


exacerbation.

TREATMENT

COPD Treatment
Acute



feelings.[27] [91]
Primary options

TREATMENT

and response

51
COPD Treatment
Acute
adjunct phosphodiesterase-4 inhibitor
Primary options
» roflumilast: 500 micrograms orally once

daily
» Roflumilast may be considered in patients

with an FEV1 <50% predicted and chronic
bronchitis,[112] especially if they have
experienced at least one hospitalization for an
exacerbation in the previous year.[27] [113]
adjunct macrolide antibiotic
Primary options
» azithromycin: 250 mg orally once daily; or

500 mg orally three times weekly
OR
» erythromycin base: 500 mg orally twice

daily
» The use of azithromycin is supported by the

best available evidence.[114] [115]
» Decision making should take into account the

potential development of resistant organisms.
TREATMENT

COPD Treatment
Acute

6[B]Evidence



TREATMENT

53
COPD Treatment
Acute
and COPD.[101]
2nd long-acting beta-2 agonist (LABA) plus
inhaled corticosteroid (ICS)
Primary options

daily
OR

twice daily
OR

OR

» In group D patients who develop further

exacerbations while taking a combination of a
LABA and a long-acting muscarinic antagonist
(LAMA), the Global Initiative for Chronic
suggest two alternative pathways: escalation to
LABA/LAMA/ICS or switch to LABA/ICS.[27]
» There is no evidence that switching from

LABA/LAMA to LABA/ICS results in better
prevention of exacerbations. If LABA/ICS therapy
does not positively impact exacerbations or
symptoms, a LAMA can be added.[27]
» In some patients, initial treatment with LABA/

ICS may be the first choice. These patients may
TREATMENT
have a history and/or findings suggestive of

asthma-COPD overlap.[27]
COPD Treatment
Acute
Primary options

OR

OR


exacerbation.


TREATMENT

55
COPD Treatment
Acute


feelings.[27] [91]
Primary options

and response

TREATMENT

COPD Treatment
Acute

6[B]Evidence



TREATMENT

57
COPD Treatment
Acute
and COPD.[101]
TREATMENT
COPD Treatment
Emerging
Medical therapies
The increasing awareness of the role of inflammation in COPD has led to consideration of drugs that attack
various targets in the inflammatory cascade. Many broad-spectrum anti-inflammatory drugs are now in phase
3 development for COPD and may enter the COPD market within the next decade. Nitric oxide inhibitors,
leukotriene modifiers, and tumor necrosis factor antagonists are among these novel therapies.[116] Long-
term (≥6 months) treatment with acetylcysteine may decrease exacerbation prevalence but does not
appear to affect exacerbation rate, lung volumes, or FEV1.[117] Antiplatelet therapy is associated with
decreased all-cause mortality in patients with COPD, independent of cardiovascular risk.[118] Epidermal
growth factor receptor kinase has potential to combat mucus overproduction. Therapy to inhibit fibrosis
is being developed. There is also a search for serine proteinase and matrix metalloproteinase inhibitors
to prevent lung destruction and the subsequent development of emphysema, as well as drugs such as
retinoid that may even reverse this process.[119] HMG-CoA reductase inhibitors are emerging medications
in COPD that have been shown to improve some outcomes, with some improvement in lung function of
COPD patients with moderate to severe class.[120] Although retrospective studies showed decreased rate
and severity of exacerbations, hospitalization, and mortality in patients using statin therapy, especially in
patients with coexisting cardiovascular disease (CVD) or hyperlipidemia, a prospective study failed to prove
this benefit.[121] In a meta-analysis of randomized controlled trials of patients with COPD taking statins,
clinical outcomes were better in patients with coexisting CVD, elevated baseline C-reactive protein, or a
high cholesterol level.[122] Efficacy and safety of synthetic ghrelin hormone therapy in COPD patients with
severely decreased physical performance and cachexia is under investigation with some promising initial
results.[123] Palovarotene is a selective retinoic acid receptor gamma agonist that is under investigation for
the treatment of emphysema. It is hypothesized that retinoic acid signaling affects alveologenesis. There
have been promising results in animal studies.[124] Many combinations of inhaler therapies are being
introduced for COPD treatment. Aclidinium/formoterol is a long-acting muscarinic antagonist and long-
acting beta-2 agonist (LABA/LAMA) combination therapy that is available in some countries, but is awaiting
approval by the Food and Drug Administration (FDA) in the US.
Interventional therapies
Target lobe volume reduction, a novel technique for selective bronchoscopic lung volume resection, has now
become available. In this technique, a one-way valve is inserted into the hyperinflated and emphysematous
segment, leading to the collapse of the nonfunctional lung segment. Promising reports have been released
from case series of patients undergoing this therapy. This approach is an alternative to surgical lung volume
reduction in COPD patients who are likely to require surgery.[125] [126]
Pharmacogenomic therapy
Pharmacogenomic therapy may be important in COPD. It is important to identify the genetic factors that
determine why certain heavy smokers develop COPD and others do not. Identification of genes that
predispose to the development of COPD may provide novel therapeutic targets.[127] [128]
Club cell protein 16 augmentation

Club cell protein 16 (CC16) is mainly produced by the Club cells (formerly known as Clara cells) in the
respiratory tract epithelium. CC16 has anti-inflammatory properties in smoke-exposed lungs, and COPD
is associated with CC16 deficiency. Experimental augmentation of CC16 levels reduces inflammation and
cellular injury, and so CC16 augmentation may be a new disease-modifying treatment for COPD.[129]
TREATMENT
59
COPD Follow up
Recommendations
Monitoring
FOLLOW UP
Patients with COPD should be evaluated on a regular basis depending on the severity of disease. Mild
stable COPD patients may be followed up at 6-month intervals, while patients with severe, frequent
exacerbations and recently hospitalized patients need follow-up at 2-week to 1-month intervals. In follow-
up sessions, patients should be evaluated to determine adherence to medical regimen, response to
therapy, and disease progression. The level of dyspnea at rest and with exercise should be determined,
as well as number of exacerbations. Questionnaires such as the COPD Assessment Test (CAT) can be
used to assess symptoms. These can be found in the GOLD guidelines.[1] Smoking status and smoke
exposure should be determined at each appointment, followed by appropriate action.[1]
PFTs should be monitored at least every 3 years, to evaluate response to therapy and possible need
for change in medications. If any significant change in medication is made or if the patient is on
systemic corticosteroids, more frequent PFT monitoring is required. The GOLD guidelines recommend
measuring FEV1 by spirometry at least once a year to identify patients who are declining quickly.[1]
Oxygen saturation should be monitored and patients evaluated periodically for the need of supplemental
oxygen. Patients need to be monitored for short-term and long-term complications of COPD. Patient
weight, nutrition status, and physical activity should also be monitored. Cachexia and reduced physical
performance are indicators of a poor prognosis.
Patient instructions
All patients should be well educated about the disease course and symptoms of exacerbation or
decompensation. Their expectation of the disease, treatment, and prognosis should be realistic. It is
important to remember that no medicine has been shown to modify the long-term decline in lung function,
and the primary goal of pharmacotherapy is to control symptoms and prevent complications.
One Cochrane review found that self-management interventions that include an action plan for acute
exacerbations of COPD are associated with improvements in health-related quality of life and fewer
admissions to hospital for respiratory problems. An exploratory analysis found a small, but significantly
higher, respiratory-related mortality rate for self-management compared to usual care, although no excess
risk of all-cause mortality was seen.[71]
One randomised controlled trial found that a telephone health coaching intervention to promote behaviour
change in patients with mild COPD in primary care led to improvements in self-management activities, but
did not improve health-related quality of life.[72]
Patients should stay as healthy and active as possible. It is necessary to stop active or passive smoking
and avoid environmental exposure to toxic fumes.
Regular medical follow-up is necessary to optimize the treatment. If there is any worsening of symptoms,
immediate medical attention is required. Patients on continuous oxygen therapy may need increase in
oxygen flow during air travel.
Physical activity is recommended for all patients with COPD and they should be encouraged to maintain
it.[1] One systematic review and meta-analysis of randomised controlled trials found that exercise training
on its own can improve physical activity in COPD, and greater improvements can be made with the
addition of physical activity counseling.[90] Another systematic review and meta-analysis found that
a combination of aerobic exercise and strength training was more effective than strength training or
endurance training alone in increasing the 6-minute walking distance.[91]
COPD Follow up
Complications
Complications Timeframe Likelihood
FOLLOW UP
cor pulmonale long term high
Cor pulmonale is right-sided heart failure secondary to longstanding COPD. It is caused by chronic
hypoxia and subsequent vasoconstriction in pulmonary vasculature that causes pulmonary hypertension
and right-sided heart failure.
Engorged neck veins, a loud P2, lower-extremity edema, and hepatomegaly are signs of cor pulmonale.
Continuous oxygen therapy is the mainstay of therapy. Judicious use of diuretics is warranted.[144]
recurrent pneumonia variable high
Recurrent pneumonia is a common complication of COPD and a frequent cause of COPD exacerbation.
Either viral or bacterial infections can be the cause.
Chronic lung and airway damage, inflammation, compromised ciliary function, and bacterial colonization
are likely causes of increased vulnerability to infections. Use of long-term inhaled corticosteroids is also
associated with increased risk of pneumonia in patients with COPD.[141] [142]
Use of antibiotic therapy has shown some benefit.[143] Usual treatment time is around 7 to 14 days.
Appropriate coverage for Haemophilus influenzae and Streptococcus pneumoniae is mandatory.
Pneumococcal vaccination is strongly recommended in COPD patients.
depression variable high
Depression is a common consequence of COPD. If any mood change occurs, a psychiatric evaluation may
be necessary.
pneumothorax variable medium
Occurs because of lung parenchyma damage with subpleural bulla formation and rupture. Spontaneous
pneumothorax is very common with chronic severe cough or chest trauma, and may be life-threatening.
High levels of suspicion are necessary for prompt diagnosis. CXR or chest CT confirms the diagnosis.
[Fig-4]
Conservative management may be sufficient in minor cases. In severe cases, chest tube insertion is
necessary to prevent tension pneumothorax and hemodynamic instability. If recurrent pneumothorax
occurs, then surgical interventions, such as video-assisted thoracoscopy pleurodesis or bullectomy, are
warranted.
respiratory failure variable medium
A study of a large number of COPD patients with acute respiratory failure reported inhospital mortality
of 17% to 49%.[140] Therapy includes noninvasive positive pressure ventilation and/or mechanical
ventilation.
anemia variable medium
61
COPD Follow up
Complications Timeframe Likelihood

Anemia is more prevalent than previously thought, affecting almost 25% of COPD patients.[145] A low
hematocrit indicates a poor prognosis in COPD patients receiving long-term oxygen treatment.[146]
FOLLOW UP
polycythemia variable medium
Secondary polycythemia can develop in the presence of arterial hypoxemia, especially in continuing
smokers. It can be identified by hematocrit >55%. Many times these patients require supplemental home
oxygen.
Prognosis
COPD is a disease with an indeterminate course and variable prognosis. Its prognosis depends on several
factors including genetic predisposition, environmental exposures, comorbidities and, to a lesser degree,
acute exacerbations.
Although short-term survival for patients with COPD and respiratory failure depends on the overall severity
of acute illness, long-term survival is primarily influenced by the severity of COPD and the presence of
comorbid conditions. Traditionally, prognosis has been reported based on the FEV1, which is a part of
pulmonary function testing. A meta-regression analysis showed a significant correlation between increased
FEV1 and lower risk of COPD exacerbation.[133] In addition to the FEV1, other factors that predict prognosis
are weight (very low weight is a negative prognostic factor[134]), distance walked in 6 minutes, and degree
of shortness of breath with activities. These factors, known as the Body mass index, airflow Obstruction,
Dyspnea, and Exercise (BODE) index, can be used to provide information on prognosis for 1-year, 2-
year, and 4-year survival.[135] One study revealed that plasma pro-adrenomedullin concentration plus
BODE index is a better prognostic tool than BODE index alone.[136] Elevation of adrenomedullin, arginine
vasopressin, atrial natriuretic peptide, and C-reactive protein[137] is associated with increased risk of
death in patients with stable COPD.[138] Recently, more interest has been put on comorbidities and prior
exacerbations as the predictor of COPD course. CODEX index (comorbidities, obstruction, dyspnea,
and previous severe exacerbations) is proved to be superior to BODE index in predicting prognosis for
COPD patients.[139] Frequent COPD exacerbations and requirement for multiple intubation and invasive
mechanical ventilation for acute respiratory failure in COPD patients are markers of poor prognosis.[140]
Among different therapeutic modalities in COPD, the only two factors that improve survival are smoking
cessation and oxygen supplementation.
[VIDEO: BODE Index for COPD Survival Prediction ]
COPD Guidelines
Diagnostic guidelines
International
Global strategy for the diagnosis, management, and prevention of COPD [26]
Published by: Global Initiative for Chronic Obstructive Lung Disease Last published: 2019
Treatment guidelines
International
Global strategy for the diagnosis, management, and prevention of COPD [27]
Published by: Global Initiative for Chronic Obstructive Lung Disease Last published: 2018
GUIDELINES
Enhancing implementation, use, and delivery of pulmonary rehabilitation
[130]
Published by: American Thoracic Society; European Respiratory Last published: 2015
Society
BTS/ICS guidelines for the ventilatory management of acute hypercapnic

respiratory failure in adults [131]
Published by: British Thoracic Society; Intensive Care Society Last published: 2017
Nursing care of dyspnea: the 6th vital sign in individuals with chronic
obstructive pulmonary disease (COPD) [132]
Published by: Registered Nurses Association of Ontario Last published: 2010
63
COPD Evidence scores
Evidence scores
1. Reduction in exacerbations: there is good-quality evidence that a combination of an anticholinergic
plus a short-acting beta-2 agonist is more effective than a short-acting beta-2 agonist alone at
reducing COPD exacerbations at 12 weeks. This combination does not seem to be more effective at
reducing exacerbations compared with an anticholinergic alone.
Evidence level A: Systematic reviews (SRs) or randomized controlled trials (RCTs) of >200
participants.
2. Lung function: there is good-quality evidence that smoking cessation interventions are more effective
than usual care at improving FEV1 in people with COPD at 1 to 5 years and at reducing all-cause
mortality at 14.5 years.
participants.
3. Reduction in exacerbations: there is good-quality evidence that beta-2 agonists are more effective than
placebo at reducing exacerbations at 12 to 52 weeks.
participants.
4. Lung function: there is medium-quality evidence that ipratropium, a short-acting anticholinergic, is

more effective than placebo at improving FEV1 at 12 weeks.
Evidence level B: Randomized controlled trials (RCTs) of <200 participants, methodologically
flawed RCTs of >200 participants, methodologically flawed systematic reviews (SRs) or good quality
observational (cohort) studies.
5. Lung function: there is good-quality evidence that theophylline is more effective than placebo at
increasing FEV1. However, its usefulness is limited by adverse effects and the need for frequent
monitoring of blood concentrations.
participants.
6. Mortality: there is medium-quality evidence that domiciliary oxygen treatment is more effective than
no oxygen supplementation at reducing mortality in people with severe daytime hypoxemia, with
continuous oxygen being more effective than nocturnal domiciliary oxygen treatment.
Evidence level B: Randomized controlled trials (RCTs) of <200 participants, methodologically
flawed RCTs of >200 participants, methodologically flawed systematic reviews (SRs) or good quality
EVIDENCE SCORES
observational (cohort) studies.
7. Lung function: there is good-quality evidence that short-acting beta-2 agonists are more effective than
placebo at increasing FEV1 and at improving daily breathlessness scores at 1 week.
COPD Evidence scores
participants.
EVIDENCE SCORES
65
COPD References
Key articles
• Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis,
REFERENCES
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Full text
• Ford ES, Croft JB, Mannino DM, et al. COPD surveillance - United States, 1999-2011. Chest. 2013
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• Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smoking intervention and the use of an inhaled
anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA. 1994 Nov
16;272(19):1497-505. Abstract
• Siafakas NM, Vermeire P, Pride NB, et al. Optimal assessment and management of chronic
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1995 Aug;8(8):1398-420. Full text Abstract
• Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis,
Full text
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77
COPD Images
Images
IMAGES
Figure 1: COPD chest x-ray (AP view): hyperinflated lung, flattened diaphragm, increased intercostal spaces
From the collection of Manoochehr Abadian Sharifabad, MD
COPD Images
IMAGES
Figure 2: COPD chest x-ray (lateral view): hyperinflated lung, flattened diaphragm, increased antero-posterior
diameter (barrel chest) in lateral view
79
IMAGES COPD Images
Figure 3: COPD chest CT: hyperinflated lung, emphysematous changes, and increased antero-posterior
diameter (barrel chest)
COPD Images
IMAGES
Figure 4: Chest CT: severe COPD changes with right pneumothorax
81
COPD Disclaimer
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DISCLAIMER
Contributors:
// Authors:
Manoochehr Abadian Sharifabad, MD

Fountain Valley Regional Medical Center
Fountain Valley, CA
DISCLOSURES: MAS declares that he has no competing interests.
// Acknowledgements:
Dr Manoochehr Abadian Sharifabad would like to gratefully acknowledge Dr Jonathan P. Parsons and
Dr Michael Ezzie, the previous contributors to this topic. JPP has contributed at speakers' bureaus for
GlaxoSmithKline, Inc., Schering-Plough, Inc., and AstraZeneca, Inc. ME declares that he has no competing
interests.
// Peer Reviewers:
Hormoz Ashtyani, MD, FCCP

Hackensack University Medical Center
Hackensack, NJ
DISCLOSURES: HA declares that he has no competing interests.
William Janssen, MD
Assistant Professor of Medicine
National Jewish Medical and Research Center, University of Colorado Health Sciences Center, Denver, CO
DISCLOSURES: WJ declares that he has no competing interests.
Francis Thien, MD, FRACP, FCCP

Associate Professor
Director of Respiratory Medicine, Eastern Health & Monash University, Victoria, Australia
DISCLOSURES: FT declares that he has no competing interests.

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COPD

The right clinical information, right where it's needed

Last updated: Sep 12, 2019

◊ Treatment options include bronchodilators, inhaled corticosteroids, and systemic corticosteroids.

◊ Long-term oxygen therapy improves survival in severe COPD.

Physical activity is recommended for all patients with COPD.[1]

Step-by-step diagnostic approach

[VIDEO: Radial artery puncture animated demonstration ]

developmentally abnormal lung

low socioeconomic status

History & examination factors

shortness of breath (common)

Other diagnostic factors

hyperresonance on percussion (common)

distant breath sounds on auscultation (common)

poor air movement on auscultation (common)

wheezing on auscultation (common)

coarse crackles (common)

distended neck veins (uncommon)

lower-extremity swelling (uncommon)

hepatojugular reflux (uncommon)

CBC elevated hematocrit,

Other tests to consider

Condition Differentiating signs / Differentiating tests

Congestive heart failure • Usually a history of • B-type natriuretic peptide

Bronchiectasis • There may be a history • Chest CT reveals bronchial

Tuberculosis • A history of fever, night • The diagnosis requires

Bronchiolitis • Bronchiolitis may affect • PFTs in bronchiolitis can

Condition Differentiating signs / Differentiating tests

Chronic sinusitis/ • Chronic sinusitis/rhinitis is • CT of sinuses and/or empiric

Gastroesophageal reflux • Patients with GERD often • Diagnosis is usually based

ACE inhibitor-induced • ACE inhibitors can cause • Diagnosis is usually

Lung cancer • Patients may have weight • Radiography is important

In pulmonary function testing, a postbronchodilator FEV1/FVC ratio of <0.70 is commonly considered

• GOLD 1 - mild: FEV1≥ 80% predicted

Step-by-step treatment approach

Continuous assessment and monitoring of disease

Exposure to risk factors and preventive measures:

• Decline in exercise tolerance

• How often rescue inhaler is used

• Urgent care or emergency room visits

• Assessment of coexisting medical problems (e.g., heart failure).

Chronic management: stepwise therapy according to Global

Bronchodilator therapy options

Umeclidinium/vilanterol is a LABA/LAMA approved for use in COPD.[46] Glycopyrrolate/formoterol

Combined bronchodilator and corticosteroid preparations

Patient education and self-management

Smoking cessation and vaccination

or environmental tobacco smoke exposures.

GOLD guidelines recommend pulmonary rehabilitation for patient groups B to D.[27]

Criteria for referral for lung transplantation include:[98]

• Progressive disease, despite maximal treatment including medication, pulmonary rehabilitation,

[VIDEO: BODE Index for COPD Survival Prediction ]

Treatment details overview

1st short- or long-acting bronchodilator

plus patient education and vaccination

plus smoking cessation

group B: more symptoms and low

1st long-acting bronchodilator

plus short-acting bronchodilator as required

plus patient education and vaccination

plus smoking cessation

plus pulmonary rehabilitation

adjunct long-term ox ygen therapy