/clinical/,/clinical/cckm-tools/,/clinical/cckm-tools/content/,/clinical/cckm-tools/content/cpg/,/clinical/cckm-tools/content/cpg/respiratory/,

/clinical/cckm-tools/content/cpg/respiratory/name-97739-en.cckm

201706181

page

100

UWHC,UWMF,

Tools,

Clinical Hub,UW Health Clinical Tool Search,UW Health Clinical Tool Search,Clinical Practice Guidelines,Respiratory

Chronic Obstructive Lung Disease (COPD) - Adult - Inpatient/Ambulatory

Chronic Obstructive Lung Disease (COPD) - Adult - Inpatient/Ambulatory - Clinical Hub, UW Health Clinical Tool Search, UW Health Clinical Tool Search, Clinical Practice Guidelines, Respiratory


1
Chronic Obstructive Pulmonary Disease –
Adult – Inpatient/Ambulatory
Clinical Practice Guideline
Table of Contents
EXECUTIVE SUMMARY ........................................................................................................... 2
PERTINENT UWHC INFORMATION ......................................................................................... 3
GLOBAL INITIATIVE FOR CHRONIC OBSTRUCTIVE LUNG DISEASE (GOLD): POCKET
GUIDE TO COPD DIAGNOSIS, MANAGEMENT, AND PREVENTION .................................... 4
APPENDIX- COPD MEDICATIONS
Guideline Contact for
Content Changes:
Richard Cornwell, MD
T: 608.263.9356
Email: rdcornwe@wisc.edu


Guideline Contact for
Document Changes:
Lindsey Spencer, MS- CCKM
T: 608.890.6403
Email: lspencer2@uwhealth.org
Guideline Author(s): 2013 Global Initiative for Chronic Obstructive Lung
Disease (GOLD) Inc.
Coordinating Team Members: Richard Cornwell, MD (Pulmonary Medicine);
Mark Regan, MD (Pulmonary Medicine); Julianne Falleroni, MD (Primary Care);
Shachar Peles, MD (Hospital Medicine); Jeff Pothof, MD (Emergency Medicine);
Philip Trapskin (Pharmacy); Catherine Decker (Pharmacy); Josh Vanderloo
(Pharmacy); Kris Ostrander (Respiratory Therapy); Jennifer Bellehumeur
(Ambulatory Nursing); Kristen Stine (Inpatient Nursing); Cindy Leeder (Patient
Education); Cara Winsand (Unity); Kim Volberg (Dean); Julie Utter (Dean); Jody
Jardine (Physicians Plus).
Review Individuals/Bodies: None
Note: Active Table of Contents
Click to follow link
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 01/2014CCKM@uwhealth.org

2
Committee Approvals: Clinical Knowledge Management Council
Release Date: 1/23/2014
Executive Summary
Chronic Obstructive Pulmonary Disease (COPD), the fourth leading cause of death
in the world, represents an important public health challenge that is preventable and
treatable.1 To address the prevention and treatment of COPD at UW Health, the COPD
guideline coordinating team has chosen to adopt the 2013 Global Initiative for Chronic
Obstructive Lung Disease, Inc. (GOLD) Pocket Guide to COPD Diagnosis,
Management, and Prevention: A Guide for Health Care Professionals1, which is a
summary of the key recommendations from the GOLD Global Strategy for the
Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease.2
Worldwide, the most commonly encountered risk factor for COPD is tobacco smoking.
In many countries, outdoor, occupational, and indoor air pollution – the latter
resulting from the burning of biomass fuels – are also major COPD risk factors.
A clinical diagnosis of COPD should be considered in any patient who has dyspnea,
chronic cough or sputum production, and a history of exposure to risk factors for the
disease. Spirometry is required to make the diagnosis in this clinical context.
Assessment of COPD is based on the patient’s symptoms, risk of exacerbations, the
severity of the spirometric abnormality, and the identification of comorbidities.
Appropriate pharmacologic therapy can reduce COPD symptoms, reduce the
frequency and severity of exacerbations, and improve health status and exercise
tolerance.
Formation and Doses of Common COPD Medications
All COPD patients with breathlessness when walking at their own pace on level ground
appear to benefit from rehabilitation and maintenance of physical activity.
An exacerbation of COPD is an acute event characterized by a worsening of the
patient’s respiratory symptoms that is beyond normal day-to-day variations and leads to
a change in medication.
COPD often coexists with other diseases (comorbidities) that may have a significant
impact on prognosis.
Note: Active Links
Click to follow link
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 01/2014CCKM@uwhealth.org

3
Pertinent UWHC Information
Policies & Procedures
Respiratory Care Protocol Policy – COPD Exacerbation Inpatient Algorithm
https://uconnect.wisc.edu/servlet/Satellite?cid=1126675766901&pagename=B_EXTRA
NET_UWH_HOME%2FFlexMemberFile%2FLoad_File&c=FlexMemberFile
Non-Invasive Assisted Ventilation
https://uconnect.wisc.edu/servlet/Satellite?cid=1093039728161&pagename=B_EXTRA
NET_UWHC_POLICIES%2FFlexMember%2FShow_Policy&c=FlexMember
Pulmonary Function Lab – Spirometry Orders
https://uconnect.wisc.edu/servlet/Satellite?cid=1119964166156&pagename=B_EXTRA
NET_UWHC_DEPARTMENTS%2FPage%2FShow_Department&c=Page
Respiratory Care Policy 3.20 – Continuous Oximetry
https://uconnect.wisc.edu/servlet/Satellite?cid=1095721190737&pagename=B_EXTRA
NET_UWHC_POLICIES%2FFlexMember%2FShow_Policy&c=FlexMember
Respiratory Care Policy 3.21 – Overnight Oximetry
https://uconnect.wisc.edu/servlet/Satellite?cid=1126650780278&pagename=B_EXTRA
NET_UWHC_POLICIES%2FFlexMember%2FShow_Policy&c=FlexMember
Benefits/Harms of Implementation
Potential Benefits: Effective diagnosis, management, and prevention of
COPD and improved cost effectiveness of therapy.
Potential Harms: Adverse side effects from use of medications.
Implementation Tools/Plan
1. This guideline will be housed in U-Connect in a dedicated folder for Clinical
Practice Guidelines.
2. Advertise release of this guideline in the Center for Knowledge Management
corner within the Best Practices Newsletter.
3. Order sets will be reviewed to ensure consistency with guidelines.
Disclaimer
CPGs are described to assist clinicians by providing a framework for the evaluation and
treatment of patients. This Clinical Practice Guideline outlines the preferred approach
for most patients. It is not intended to replace a clinician’s judgment or to establish a
protocol for all patients. It is understood that some patients will not fit the clinical
condition contemplated by a guideline and that a guideline will rarely establish the only
appropriate approach to a problem.
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 01/2014CCKM@uwhealth.org

4
References
1. This Pocket Guide has been developed from the Global Strategy for the Diagnosis,
Management, and Prevention of COPD (Updated 2013). This document is
included here with permission from the Global Initiative for Chronic Obstructive Lung
Disease, Inc. 2013. http://www.goldcopd.org/guidelines-pocket-guide-to-copd-
diagnosis.html
2. From the Global Strategy for the Diagnosis, Management and Prevention of COPD,
Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2013. Available from:
http://www.goldcopd.org/.
Global Initiative for Chronic Obstructive Lung Disease
(GOLD): Pocket Guide to COPD Diagnosis, Management, and
Prevention
Copyright © 2014 Univ ersity of Wisconsin Hospitals and Clinics Authority
Contact: Lee Vermeulen, CCKM@uwhealth.org Last Revised: 01/2014CCKM@uwhealth.org

Global Initiative for Chronic
Obstructive
Lung
Disease
Global Initiative for Chronic
Obstructive
Lung
Disease
POCKET GUIDE TO
COPD DIAGNOSIS, MANAGEMENT,
AND PREVENTION
A Guide for Health Care Professionals
UPDATED 2013

Global Initiative for Chronic
Obstructive
Lung
Disease
Pocket Guide to COPD Diagnosis, Management,
And Prevention, 2013
GOLD Board of Directors
Marc Decramer, MD, Chair Jean Bourbeau, MD
Katholieke Universiteit Leuven McGill University Health Centre
Leuven, Belgium Montreal, Quebec, Canada

Jorgen Vestbo, MD, Vice Chair Bartolome R. Celli, MD
Odense University Hospital Brigham and Women’s Hospital
Odense C, Denmark (and) Boston, Massachusetts USA
University of Manchester
Manchester, UK M.Victorina López Varela, MD
Universidad de la Repúblic
David S.C. Hui, MD Montevideo, Uruguay
The Chinese University of Hong Kong
Hong Kong, ROC Roberto Rodriguez Roisin, MD
Hospital Clínic, University of Barcelona
Masaharu Nishimura, MD Barcelona, Spain
Hokkaido University School of Medicine
Sapporo, Japan Claus Vogelmeier, MD
University of Gießen and Marburg
Robert A. Stockley Marburg, Germany
University Hospitals Birmingham
Birmingham, UK

GOLD Science Committee
Jørgen Vestbo, MD, Denmark, UK, Chair Fernando Martinez, MD, USA
Alvar Agusti, MD, Spain Masaharu Nishimura, MD, Japan
Antonio Anzueto, MD, USA Nicolas Roche, MD, France
Peter J. Barnes, MD, UK Roberto Rodriguez Roisin, MD, Spain
Marc Decramer, MD, Belgium Donald Sin, MD, Canada
Leonardo M. Fabbri, MD, Italy Robert A. Stockley, MD, UK
Paul Jones, MD, UK Claus Vogelmeier, MD, Germany

GOLD Science Director
Suzanne Hurd, PhD, USA

GOLD National Leaders

Representatives from many countries serve as a network for the dissemination and
implementation of programs for diagnosis, management, and prevention of COPD. The
GOLD Board of Directors is grateful to the many GOLD National Leaders who participated in
discussions of concepts that appear in GOLD reports.
2013 Global Initiative for Chronic Obstructive Lung Disease, Inc.

TABLE OF CONTENTS
3 INTRODUCTION
4 KEY POINTS
5 WHAT IS CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)?
6 WHAT CAUSES COPD?
7 DIAGNOSIS OF COPD
7 ? Table 1: Key Indicators for Considering a
Diagnosis of COPD
8 ? Table 2: COPD and its Differential Diagnoses
9 ASSESSMENT OF COPD
9 ? Table 3: Classification of Severity of Airflow
Limitation in COPD
10 ? Table 4: Combined Assessment of COPD
11 THERAPEUTIC OPTIONS
14 ? Table 5: Formulations and Typical Doses of
COPD Medications
17 MANAGEMENT OF STABLE COPD
17 ? Table 6: Non-Pharmacologic Management of COPD
19 ? Table 7: Pharmacologic Therapy for Stable COPD
20 MANAGEMENT OF EXACERBATIONS
21 ? Table 8: Indications for Hospital Assessment
or Admission
22 COPD AND COMORBIDITIES
23 APPENDIX I: SPIROMETRY FOR DIAGNOSIS OF AIRLOW LIMITATION
IN COPD
24 ? Figure 1A: Normal Spirogram
24 ? Figure 1B: Spirogram Typical of Patients with
Mild to Moderate COPD

3
INTRODUCTION
Chronic Obstructive Pulmonary Disease (COPD) is a major cause of morbidity
and mortality throughout the world. Much has been learned about COPD
since the Global Initiative for Chronic Obstructive Lung Disease issued its first
report, Global Strategy for the Diagnosis, Management, and Prevention of
COPD, in 2001. Treatment of COPD is now aimed at immediately relieving
and reducing the impact of symptoms, as well as reducing the risk of future
adverse health events such as exacerbations. These dual goals emphasize
the need for clinicians to maintain a focus on both the short-term and long-
term impact of COPD on their patients. A framework for COPD management
that matches individualized assessment of the disease to these treatment
objectives will better meet each patient’s needs.
Several educational tools and publications oriented around this approach to
COPD are available at http://www.goldcopd.org and can be adapted to
local health care systems and resources:
? Global Strategy for the Diagnosis, Management, and Prevention
of COPD. Scientific information and recommendations for COPD
programs. (Updated 2013)
? Executive Summary, Global Strategy for the Diagnosis, Management,
and Prevention of COPD. American Journal of Respiratory and Critical
Care Medicine (in press).
? Pocket Guide to COPD Diagnosis, Management, and Prevention.
Summary of patient care information for primary health care
professionals. (Updated 2013)
? What You and Your Family Can Do About COPD. Information booklet
for patients and their families.
This Pocket Guide has been developed from the Global Strategy for the
Diagnosis, Management, and Prevention of COPD (Updated 2013). Technical
discussions of COPD and COPD management, evidence levels, and specific
citations from the scientific literature are included in that source document.
Acknowledgements: Unconditional educational grants have been provided
by Almirall, AstraZeneca, Boehringer-Ingelheim, Chiesi, Forest Laboratories,
GlaxoSmithKline, Groupo Ferrer, Merck Sharp & Dohme, Mylan, Nonin
Medical, Novartis, Pearl Therapeutics, Pfizer, Quintiles, and Takeda. The
participants of the GOLD committees, however, are solely responsible for the
statements and conclusions in the publications.

4
KEY POINTS
? Chronic Obstructive Pulmonary Disease (COPD), a common preventable
and treatable disease, is characterized by persistent airflow limitation
that is usually progressive and associated with an enhanced chronic
inflammatory response in the airways and the lung to noxious particles
or gases. Exacerbations and comorbidities contribute to the overall
severity in individual patients.
? Worldwide, the most commonly encountered risk factor for COPD is
tobacco smoking. In many countries, outdoor, occupational, and indoor
air pollution – the latter resulting from the burning of biomass fuels – are
also major COPD risk factors.
? A clinical diagnosis of COPD should be considered in any patient who
has dyspnea, chronic cough or sputum production, and a history of
exposure to risk factors for the disease. Spirometry is required to make
the diagnosis in this clinical context.
? Assessment of COPD is based on the patient’s symptoms, risk of
exacerbations, the severity of the spirometric abnormality, and the
identification of comorbidities.
? Appropriate pharmacologic therapy can reduce COPD symptoms,
reduce the frequency and severity of exacerbations, and improve health
status and exercise tolerance.
? All COPD patients with breathlessness when walking at their own pace
on level ground appear to benefit from rehabilitation and maintenance
of physical activity.
? An exacerbation of COPD is an acute event characterized by a
worsening of the patient’s respiratory symptoms that is beyond normal
day-to-day variations and leads to a change in medication.
? COPD often coexists with other diseases (comorbidities) that may have
a significant impact on prognosis.

5
WHAT IS CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE (COPD)?
Chronic Obstructive Pulmonary Disease (COPD), a common preventable and
treatable disease, is characterized by persistent airflow limitation that is usually
progressive and associated with an enhanced chronic inflammatory response
in the airways and the lung to noxious particles or gases. Exacerbations and
comorbidities contribute to the overall severity in individual patients.
This definition does not use the terms chronic bronchitis and emphysema*
and excludes asthma (reversible airflow limitation).
Symptoms of COPD include:
? Dyspnea
? Chronic cough
? Chronic sputum production
Episodes of acute worsening of these symptoms (exacerbations) often occur.
Spirometry is required to make a clinical diagnosis of COPD; the presence of
a post-bronchodilator FEV
1
/FVC < 0.70 confirms the presence of persistent
airflow limitation and thus of COPD.
*Chronic bronchitis, defined as the presence of cough and sputum production for at least 3
months in each of 2 consecutive years, is not necessarily associated with airflow limitation.
Emphysema, defined as destruction of the alveoli, is a pathological term that is sometimes
(incorrectly) used clinically and describes only one of several structural abnormalities present
in patients with COPD – but can also be found in subjects with normal lung function.

6
WHAT CAUSES COPD?
Worldwide, the most commonly encountered risk factor for COPD is
tobacco smoking. Outdoor, occupational, and indoor air pollution – the
latter resulting from the burning of biomass fuels – are other major COPD
risk factors. Nonsmokers may also develop COPD.
The genetic risk factor that is best documented is a severe hereditary
deficiency of alpha-1 antitrypsin. It provides a model for how other genetic
risk factors are thought to contribute to COPD.
COPD risk is related to the total burden of inhaled particles a person
encounters over their lifetime:
? Tobacco smoke, including cigarette, pipe, cigar, and other
types of tobacco smoking popular in many countries, as well as
environmental tobacco smoke (ETS)
? Indoor air pollution from biomass fuel used for cooking and heating
in poorly vented dwellings, a risk factor that particularly affects
women in developing countries
? Occupational dusts and chemicals (vapors, irritants, and fumes)
when the exposures are sufficiently intense or prolonged
? Outdoor air pollution also contributes to the lungs’ total burden of
inhaled particles, although it appears to have a relatively small
effect in causing COPD
In addition, any factor that affects lung growth during gestation and
childhood (low birth weight, respiratory infections, etc.) has the potential to
increase an individual’s risk of developing COPD.

7
DIAGNOSIS OF COPD
A clinical diagnosis of COPD should be considered in any patient who has
dyspnea, chronic cough or sputum production, and a history of exposure to
risk factors for the disease (Table 1).
Spirometry is required to make a clinical diagnosis of COPD; the presence of
a postbronchodilator FEV
1
/FVC < 0.70 confirms the presence of persistent
airflow limitation and thus of COPD. All health care workers who care for
COPD patients should have access to spirometry. Appendix I: Spirometry
for Diagnosis of Airflow Limitation in COPD summarizes the lung function
measurements that are key to making a spirometry diagnosis and details
some of the factors needed to achieve accurate test results.
Table 1. Key Indicators for Considering a Diagnosis of COPD
Consider COPD, and perform spirometry, if any of these indicators are
present in an individual over age 40. These indicators are not diagnostic
themselves, but the presence of multiple key indicators increases the
probability of a diagnosis of COPD. Spirometry is required to establish a
diagnosis of COPD.
Dyspnea that is: Progressive (worsens over time).
Characteristically worse with exercise.
Persistent.

Chronic cough: May be intermittent and may be unproductive.

Chronic sputum production:
Any pattern of chronic sputum production may
indicate COPD.
History of exposure to risk factors:
Tobacco smoke (including popular local preparations).
Smoke from home cooking and heating fuels.
Occupational dusts and chemicals.
Family history of COPD

8
Differential Diagnosis: A major differential diagnosis is asthma. In some
patients with chronic asthma, a clear distinction from COPD is not possible
using current imaging and physiological testing techniques. In these patients,
current management is similar to that of asthma. Other potential diagnoses
are usually easier to distinguish from COPD (Table 2).
Table 2. COPD and its Differential Diagnoses
Diagnosis Suggestive Features
COPD Onset in mid-life.
Symptoms slowly progressive.
History of tobacco smoking or exposure to other types of smoke.
Asthma Onset early in life (often childhood).
Symptoms vary widely from day to day.
Symptoms worse at night/early morning.
Allergy, rhinitis, and/or eczema also present.
Family history of asthma.
Congestive Heart
Failure
Chest X-ray shows dilated heart, pulmonary edema.
Pulmonary function tests indicate volume restriction,
not airflow limitation.
Bronchiectasis Large volumes of purulent sputum.
Commonly associated with bacterial infection.
Chest X-ray/CT shows bronchial dilation, bronchial wall thickening.
Tuberculosis Onset all ages.
Chest X-ray shows lung infiltrate.
Microbiological confirmation.
High local prevalence of tuberculosis.
Obliterative
Bronchiolitis
Onset at younger age, nonsmokers.
May have history of rheumatoid arthritis or acute fume exposure.
Seen after lung or bone marrow transplantation.
CT on expiration shows hypodense areas.
Diffuse Panbronchiolitis Predominantly seen in patients of Asian descent.
Most patients are male and nonsmokers.
Almost all have chronic sinusitis.
Chest X-ray and HRCT show diffuse small centrilobular nodular
opacities and hyperinflation.
These features tend to be characteristic of the respective diseases, but are not
mandatory. For example, a person who has never smoked may develop COPD
(especially in the developing world where other risk factors may be more important
than cigarette smoking); asthma may develop in adult and even in elderly patients.

9
ASSESSMENT OF COPD
The goals of COPD assessment are to determine the severity of the disease, its
impact on patient’s health status, and the risk of future events (exacerbations,
hospital admissions, death) in order to guide therapy. Assess the following
aspects of the disease separately:
? Symptoms
? Degree of airflow limitation (using spirometry)
? Risk of exacerbations
? Comorbidities
Assess Symptoms: Validated questionnaires such as the COPD Assessment Test
(CAT), the Modified British Medical Research Council (mMRC) breathlessness
scale, or the Clinical COPD Questionnaire (CCQ) should be used to assess
symptoms.
Assess Degree of Airflow Limitation Using Spirometry: Table 3 provides the
classification of airflow limitation severity in COPD.
Assess Risk of Exacerbations: An exacerbation of COPD is defined as an acute
event characterized by a worsening of the patient’s respiratory symptoms that
is beyond normal day-to-day variations and leads to a change in medication.
The best predictor of having frequent exacerbations (2 or more per year) is a
history of previous treated events; the risk of exacerbations also increases as
airflow limitation worsens.
Assess Comorbidities: Cardiovascular diseases, osteoporosis, depression and
Table 3. Classification of Severity of Airflow Limitation in COPD
(Based on Post-Bronchodilator FEV
1
)
In patients with FEV
1
/FVC < 0.70:
GOLD 1: Mild FEV
1
≥ 80% predicted
GOLD 2: Moderate 50% ≤ FEV
1
< 80% predicted
GOLD 3: Severe 30% ≤ FEV
1
< 50% predicted
GOLD 4: Very Severe FEV
1
< 30% predicted

10
anxiety, skeletal muscle dysfunction, metabolic syndrome, and lung cancer
among other diseases occur frequently in COPD patients. These comorbid
conditions may influence mortality and hospitalizations, and should be looked
for routinely and treated appropriately.
Combined Assessement of COPD: Table 4 provides a rubric for combining
these assessments to improve management of COPD.
? Symptoms:
Less Symptoms (mMRC 0-1 or CAT < 10): patient is (A) or (C)
More Symptoms (mMRC ≥ 2 or CAT ≥ 10): patient is (B) or (D)
? Airflow Limitation:
Low Risk (GOLD 1 or 2): patient is (A) or (B)
High Risk (GOLD 3 or 4): patient is (C) or (D)
? Exacerbations:
Low Risk (≤ 1 per year): patient is (A) or (B)
High Risk (≥ 2 per year): patient is (C) or (D)
Table 4. Combined Assessment of COPD
When assessing risk, choose the highest risk according to GOLD grade or exacerbation history.
(One or more hospitalizations for COPD exacerbations should be considered high risk.)
Patient Characteristic
Spirometric
Classification
Exacerbations per
year
mMRC CAT
A
Low Risk
Less Symptoms
GOLD 1-2 ≤ 1 0-1 < 10
B
Low Risk
More Symptoms
GOLD 1-2 ≤ 1 ≥ 2 ≥ 10
C
High Risk
Less Symptoms
GOLD 3-4 ≥ 2 0-1 < 10
D
High Risk
More Symptoms
GOLD 3-4 ≥ 2 ≥ 2 ≥ 10

11
THERAPEUTIC OPTIONS
Smoking cessation has the greatest capacity to influence the natural history of
COPD. Health care providers should encourage all patients who smoke to quit.
? Counseling delivered by physicians and other health
professionals significantly increases quit rates over self-initiated
strategies. Even a brief (3-minute) period of counseling to
urge a smoker to quit results in smoking quit rates of 5-10%.
? Nicotine replacement therapy (nicotine gum, inhaler, nasal
spray, transdermal patch, sublingual tablet, or lozenge) as
well as pharmacotherapy with varenicline, bupropion, or
nortriptyline reliably increases long-term smoking abstinence
rates and these treatments are significantly more effective
than placebo.
Smoking Prevention: Encourage comprehensive tobacco-control policies and
programs with clear, consistent, and repeated nonsmoking messages. Work
with government officials to pass legislation to establish smoke-free schools,
public facilities, and work environments and encourage patients to keep smoke-
free homes.
Occupational Exposure: Emphasize primary prevention, which is best achieved
by elimination or reduction of exposures to various substances in the workplace.
Secondary prevention, achieved through surveillance and early detection, is
also important.
Indoor and Outdoor Air Pollution: Implement measures to reduce or avoid
indoor air pollution from burning biomass fuel for cooking and heating in
poorly ventilated dwellings. Advise patients to monitor public announcements
of air quality and, depending on the severity of their disease, avoid vigorous
exercise outdoors or stay indoors during pollution episodes.
Physical Activity: All COPD patients benefit from regular physical activity and
should repeatedly be encouraged to remain active.


12
PHARMACOLOGIC THERAPIES FOR STABLE COPD
Pharmacologic therapy is used to reduce symptoms, reduce the frequency and
severity of exacerbations, and improve health status and exercise tolerance.
Each treatment regimen needs to be patient-specific as the relationship between
the severity of symptoms and the severity of airflow limitation is influenced by
other factors, such as the frequency and severity of exacerbations, the presence
of respiratory failure, comorbidities (cardiovascular disease, osteoporosis,
etc.), and general health status. The classes of medications commonly used in
treating COPD are shown in Table 5. The choice within each class depends on
the availability of medication and the patient’s response.
Bronchodilators: These medications are central to symptom management in
COPD.
? Inhaled therapy is preferred.
? The choice between beta
2
-agonists, anticholinergics, theophylline,
or combination therapy depends on the availability of medications
and each patient’s individual response in terms of symptom relief
and side effects.
? Bronchodilators are prescribed on an as-needed or on a regular
basis to prevent or reduce symptoms.
? Long-acting inhaled bronchodilators are convenient and more
effective at producing maintained symptom relief than short-acting
bronchodilators.
? Long-acting inhaled bronchodilators reduce exacerbations and
related hospitalizations and improve symptoms and health status,
and tiotropium improves the effectiveness of pulmonary rehabilitation.
? Combining bronchodilators of different pharmacological classes
may improve efficacy and decrease the risk of side effects compared
to increasing the dose of a single bronchodilator.
Inhaled Corticosteroids: In COPD patients with FEV
1
< 60% predicted, regular
treatment with inhaled corticosteroids improves symptoms, lung function, and
quality of life, and reduces the frequency of exacerbations. Inhaled corticosteroid
therapy is associated with an increased risk of pneumonia. Withdrawal
from treatment with inhaled corticosteroids may lead to exacerbations in
some patients. Long-term monotherapy with inhaled corticosteroids is not
recommended.

13
Combination Inhaled Corticosteroid/Bronchodilator Therapy: An inhaled
corticosteroid combined with a long-acting beta
2
-agonist is more effective
than either individual component in improving lung function and health status
and reducing exacerbations in patients with moderate to very severe COPD.
Combination therapy is associated with an increased risk of pneumonia.
Addition of a long-acting beta
2
-agonist/inhaled glucocorticosteroid to tiotropium
appears to provide additional benefits.
Oral Corticosteroids: Long-term treatment with oral corticosteroids is not
recommended.
Phosphodiesterase-4 inhibitors: In GOLD 3 and GOLD 4 patients with a history
of exacerbations and chronic bronchitis, the phosphodiesterase-4 inhibitor
roflumilast reduces exacerbations treated with oral corticosteroids. These effects
are also seen when roflumilast is added to long-acting bronchodilators; there
are no comparison studies with inhaled corticosteroids.
Methylxanthines. Methylxanthines are less effective and less well tolerated than
inhaled long-acting bronchodilators and are not recommended if those drugs
are available and affordable. There is evidence for a modest bronchodilator
effect and some symptomatic benefit of these medications compared with
placebo in stable COPD. Addition of theophylline to salmeterol produces a
greater increase in FEV
1
and relief of breathlessness than salmeterol alone.
Low-dose theophylline reduces exacerbations but does not improve post-
bronchodilator lung function.
Other Pharmacologic Treatments
Vaccines: Influenza vaccines can reduce serious illness and death in COPD
patients. Vaccines containing killed or live, inactivated viruses are recommended,
and should be given once each year. Pneumococcal polysaccharide vaccine is
recommended for COPD patients 65 years and older, and has been shown to
reduce community-acquired pneumonia in those under age 65 with FEV
1

< 40% predicted.
Alpha-1 Antitrypsin Augmentation Therapy: Not recommended for patients
with COPD that is unrelated to alpha-1 antitrypsin deficiency.
Antibiotics: Not recommended except for treatment of infectious exacerbations
and other bacterial infections.

14
Table 5. Formulations and Typical Doses of COPD Medications*
Drug
Inhaler
(mcg)
Solution for
Nebulizer
(mg/ml)
Oral
Vials for
Injection
(mg)
Duration
of Action
(hours)
Beta
2
-agonists
Short-acting
Fenoterol 100-200 (MDI) 1 0.05% (Syrup) 4-6
Levalbuterol 45-90 (MDI) 0.21, 0.42 6-8
Salbutamol (albuterol)
100, 200
(MDI & DPI)
5
5 mg (Pill),
0.024%(Syrup)
0.1, 0.5 4-6
Terbutaline 400, 500 (DPI) 2.5, 5 mg (Pill) 4-6
Long-acting
Formoterol 4.5-12 (MDI & DPI) 0.01

12
Arformoterol 0.0075 12
Indacaterol 75-300 (DPI) 24
Salmeterol 25-50 (MDI & DPI) 12
Tulobuterol 2 mg (transdermal) 24
Anticholinergics
Short-acting
Ipratropium bromide 20, 40 (MDI) 0.25-0.5 6-8
Oxitropium bromide 100 (MDI) 1.5 7-9
Long-acting
Aclidinium bromide 322 (DPI) 12
Glycopyrronium bromide 44 (DPI) 24
Tiotropium 18 (DPI), 5 (SMI) 24
Combination short-acting beta
2
-agonists plus anticholinergic in one inhaler
Fenoterol/Ipratropium 200/80 (MDI) 1.25/0.5 6-8
Salbutamol/Ipratropium 75/15 (MDI) 0.75/0.5 12 6-8
Methylxanthines
Aminophylline 200-600 mg (Pill) 240
Variable,
up to 24
Theophylline (SR) 100-600 mg (Pill)
Variable,
up to 24
Inhaled corticosteroids
Beclomethasone 50-400 (MDI & DPI) 0.2-0.4
Budesonide 100, 200, 400 (DPI) 0.20. 0.25, 0.5
Fluticasone 50-500 (MDI & DPI)
Combination long-acting beta
2
-agonists plus corticosteroids in one inhaler
Formoterol/Budesonide
4.5/160 (MDI)
9/320 (DPI)
Formoterol/mometasone 10/200, 10/400 (MDI)
Salmeterol/Fluticasone
50/100, 250, 500 (DPI)
25/50, 125, 250 (MDI)
Systemic corticosteroids
Prednisone 5-60 mg (Pill)
Methyl-prednisolone 4, 8, 16 mg (Pill)
Phosphodiesterase-4 inhibitors
Roflumilast 500 mcg (Pill) 24
MDI=metered dose inhaler; DPI=dry powder inhaler; SMI=soft mist inhaler
*Not all formulations are available in all countries; in some countries, other formulations may be available.
¶Formoterol nebulized solution is based on the unit dose vial containing 20 mcg in a volume of 2.0 ml

15
Mucolytic Agents: Patients with viscous sputum may benefit from mucolytics
(e.g. carbocysteine), but overall benefits are very small.
Antitussives: Use is not recommended.
Vasodilators: Nitric oxide is contraindicated in stable COPD. The use of
endothelium-modulating agents for the treatment of pulmonary hypertension
associated with COPD is not recommended.
OTHER TREATMENTS
Rehabilitation: Patients at all stages of disease benefit from exercise training
programs with improvements in exercise tolerance and symptoms of dyspnea
and fatigue. Benefits can be sustained even after a single pulmonary
rehabilitation program. The minimum length of an effective rehabilitation
program is 6 weeks; the longer the program continues, the more effective the
results. Benefit does wane after a rehabilitation program ends, but if exercise
training is maintained at home the patient’s health status remains above pre-
rehabilitation levels.
Oxygen Therapy: The long-term administration of oxygen (> 15 hours per
day) to patients with chronic respiratory failure has been shown to increase
survival in patients with severe, resting hypoxemia. Long-term oxygen therapy
is indicated for patients who have:
? PaO
2
at or below 7.3 kPa (55 mmHg) or SaO
2
at or below 88%, with
or without hypercapnia confirmed twice over a three-week period; or
? PaO
2
between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg), or SaO
2

of 88%, if there is evidence of pulmonary hypertension, peripheral
edema suggesting congestive cardiac failure, or polycythemia
(hematocrit > 55%).
Ventilatory Support: The combination of non-invasive ventilation with long-term
oxygen therapy may be of some use in a selected subset of patients, particularly
in those with pronounced daytime hypercapnia. It may improve survival but
does not improve quality of life. There are clear benefits of continuous positive
airway pressure (CPAP) on both survival and risk of hospital admission.

16
Surgical Treatments: The advantage of lung volume reduction surgery (LVRS)
over medical therapy is more significant among patients with upper-lobe
predominant emphysema and low exercise capacity prior to treatment,
although LVRS is costly relative to health-care programs not including surgery.
In appropriately selected patients with very severe COPD, lung transplantation
has been shown to improve quality of life and functional capacity.
Palliative Care, End-of-life Care, and Hospice Care: The disease trajectory in
COPD is usually marked by a gradual decline in health status and increasing
symptoms, punctuated by acute exacerbations that are associated with an
increased risk of dying. Progressive respiratory failure, cardiovascular diseases,
malignancies and other diseases are the primary cause of death in patients with
COPD hospitalized for an exacerbation. Thus palliative care, end-of-life care,
and hospice care are important components of the management of patients
with advanced COPD.

17
MANAGEMENT OF STABLE COPD
Once COPD has been diagnosed, effective management should be based
on an individualized assessment of current symptoms and future risks:
? Relieve symptoms
? Improve exercise tolerance
? Improve health status
and
? Prevent disease progression
? Prevent and treat exacerbations
? Reduce mortality
These goals should be reached with minimal side effects from treatment,
a particular challenge in COPD patients because they commonly have
comorbidities that also need to be carefully identified and treated.
NON-PHARMACOLOGIC TREATMENT
Non-pharmacologic management of COPD according to the individualized
assessment of symptoms and exacerbation risk is shown in Table 6.
REDUCE SYMPTOMS
REDUCE RISK
Table 6. Non-Pharmacologic Management of COPD
Patient Group Essential Recommended
Depending on
Local Guidelines
A
Smoking
cessation
(can include
pharmacologic
treatment)
Physical activity
Flu vaccination
Pneumococcal
vaccination
B, C, D
Smoking
cessation
(can include
pharmacologic
treatment)
Pulmonary
rehabilitation
Physical activity
Flu vaccination
Pneumococcal
vaccination

18
PHARMACOLOGIC TREATMENT
A proposed model for initial pharmacological management of COPD
according to the assessment of symptoms and risk (Table 3) is shown in
Table 7.
Bronchodilators – Recommendations:
? For both beta
2
-agonists and anticholinergics, long-acting
formulations are preferred over short-acting formulations.
? The combined use of short- or long-acting beta
2
-agonists and
anticholinergics may be considered if symptoms are not improved
with single agents.
? Based on efficacy and side effects, inhaled bronchodilators are
preferred over oral bronchodilators.
? Based on evidence of relatively low efficacy and greater side
effects, treatment with theophylline is not recommended unless
other bronchodilators are not available or unaffordable for long-
term treatment.
Corticosteroids and Phosphodiesterase-4 Inhibitors – Recommendations
? There is no evidence to recommend a short-term therapeutic trial
with oral corticosteroids in patients with COPD to identify those
who will respond to inhaled corticosteroids or other medications.
? Long-term treatment with inhaled corticosteroids is recommended
for patients with severe and very severe airflow limitation and
for patients with frequent exacerbations that are not adequately
controlled by long-acting bronchodilators.
? Long-term monotherapy with oral corticosteroids is not recommended
in COPD.
? Long-term monotherapy with inhaled corticosteroids is not recommended
in COPD because it is less effective than the combination of inhaled
corticosteroids with long-acting beta
2
-agonists.
? Long-term treatment containing inhaled corticosteroids should not
be prescribed outside their indications, due to the risk of pneumonia
and the possibility of a slightly increased risk of fractures following
long-term exposure.
? The phosphodiesterase-4 inhibitor roflumilast may also be used to
reduce exacerbations for patients with chronic bronchitis, severe
and very severe airflow limitation, and frequent exacerbations that
are not adequately controlled by long-acting bronchodilators.

1
9
*Medications in each
box are mentioned in
alphabetical order and
therefore not necessarily in
order of preference.
**Medications in this
column can be used alone
or in combination with
other options in the First
and Alternative Choice
columns
Glossary:
SA: short-acting
LA: long-acting
ICS: inhaled corticosteroid
PDE-4: phosphodiesterase-4
prn: when necessary
Table 7: Pharmacologic Therapy for Stable COPD*
Patient
Group
RECOMMENDED
FIRST CHOICE
ALTERNATIVE CHOICE
OTHER POSSIBLE
TREATMENTS**
A
SA anticholinergic prn
or
SA beta
2
-agonist prn
LA anticholinergic
or
LA beta
2
-agonist
or
SA beta
2
-agonist and
SA anticholinergic
Theophylline
B
LA anticholinergic
or
LA beta
2
-agonist
LA anticholinergic and
LA beta
2
-agonist
SA beta
2
-agonist and/or
SA anticholinergic
Theophylline
C
ICS + LA beta
2
-agonist
or
LA anticholinergic
LA anticholinergic and
LA beta
2
-agonist
or
LA anticholinergic and
PDE-4 Inhibitor
or
LA beta
2
-agonist and
PDE-4 Inhibitor
SA beta
2
-agonist and/or
SA anticholinergic
Theophylline
D
ICS + LA beta
2
-agonist
and/or
LA anticholinergic
ICS + LA beta
2
-agonist and
LA anticholinergic
or
ICS + LA beta
2
-agonist and
PDE-4 inhibitor
or
LA anticholinergic and
LA beta
2
-agonist
or
LA anticholinergic and
PDE-4 inhibitor
Carbocysteine
SA beta
2
-agonist and/or
SA anticholinergic
Theophylline

20
MANAGEMENT OF
EXACERBATIONS
An exacerbation of COPD is defined as an acute event characterized by a
worsening of the patient’s respiratory symptoms that is beyond normal day-
to-day variations and leads to a change in medication.
The most common causes appear to be respiratory tract infections (viral or
bacterial).
How to Assess the Severity of an Exacerbation
? Arterial blood gas measurements (in hospital): PaO
2
< 8.0 kPa
(60 mmHg) with or without PaCO
2
> 6.7 kPa, (50 mmHg) when
breathing room air indicates respiratory failure.
? Chest radiographs are useful in excluding alternative diagnoses.
? An ECG may aid in the diagnosis of coexisting cardiac problems.
Other laboratory tests:
? Whole blood count can identify polycythemia or bleeding.
? The presence of purulent sputum during an exacerbation can be
sufficient indication for starting empirical antibiotic treatment.
? Biochemical tests can help detect electrolyte disturbances, diabetes,
and poor nutrition.
Spirometric tests are not recommended during an exacerbation because they
can be difficult to perform and measurements are not accurate enough.
Treatment Options
Oxygen: Supplemental oxygen should be titrated to improve the patient’s
hypoxemia with a target saturation of 88-92%.
Bronchodilators: Short-acting inhaled beta
2
-agonists with or without short-
acting anticholinergics are the preferred bronchodilators for treatment of an
exacerbation.

21
Systemic Corticosteroids: Systemic corticosteroids shorten recovery time,
improve lung function (FEV
1
) and arterial hypoxemia (PaO
2
), and reduce
the risks of early relapse, treatment failure, and length of hospital stay. A
dose of 30-40 mg prednisolone per day for 10-14 days is recommended.
Antibiotics: Antibiotics should be given to patients:
? With the following three cardinal symptoms: increased dyspnea,
increased sputum volume, increased sputum purulence;
? With increased sputum purulence and one other cardinal symptom;
? Who require mechanical ventilation
Adjunct Therapies: Depending on the clinical condition of the patient, an
appropriate fluid balance with special attention to the administration of
diuretics, anticoagulants, treatment of comorbidities, and nutritional aspects
should be considered. At any time, health care providers should strongly
enforce stringent measures against active cigarette smoking.
Patients with characteristics of a severe exacerbation should be hospitalized
(Table 8). Indications for referral and the management of exacerbations of
COPD in the hospital depend on local resources and the facilities of the
local hospital.
Table 8. Indications for Hospital Assessment or Admission
? Marked increase in intensity of symptoms
? Severe underlying COPD
? Onset of new physical signs
? Failure of an exacerbation to respond to initial medical management
? Presence of serious comorbidities
? Frequent exacerbations
? Older age
? Insufficient home support

22
COPD AND COMORBIDITIES
COPD often coexists with other diseases (comorbidities) that may have a
significant impact on prognosis. In general, the presence of comorbidities
should not alter COPD treatment and comorbidities should be treated as if
the patient did not have COPD.
Cardiovascular disease (including ischemic heart disease, heart failure,
atrial fibrillation, and hypertension) is a major comorbidity in COPD and
probably both the most frequent and most important disease coexisting with
COPD. Cardioselective beta-blockers are not contraindicated in COPD.
Osteoporosis and anxiety/depression, major comorbidities in COPD, are
often under-diagnosed and are associated with poor health status and
prognosis.
Lung cancer is frequently seen in patients with COPD and has been found to
be the most frequent cause of death in patients with mild COPD.
Serious infections, especially respiratory infections, are frequently seen in
patients with COPD.
The presence of metabolic syndrome and manifest diabetes are more
frequent in COPD and the latter is likely to impact on prognosis.

23
APPENDIX I: SPIROMETRY
FOR DIAGNOSIS OF AIRFLOW
LIMITATION IN COPD
Spirometry is required to make a clinical diagnosis of COPD and should
be available to all health care professionals who work with COPD patients.
What is Spirometry?
Spirometry is a simple test to measure the amount of air a
person can breathe out, and the amount of time taken to do so.
A spirometer is a device used to measure how effectively, and
how quickly, the lungs can be emptied.
A spirogram is a volume-time curve.
Spirometry measurements used for diagnosis of COPD include
(see Figures 1A and 1B):
? FVC (Forced Vital Capacity): maximum volume of air that can be
exhaled during a forced maneuver.
? FEV
1
(Forced Expired Volume in one second): volume expired in the
first second of maximal expiration after a maximal inspiration. This
is a measure of how quickly the lungs can be emptied.
? FEV
1
/FVC: FEV
1
expressed as a proportion of the FVC, gives a
clinically useful index of airflow limitation.
The ratio FEV
1
/FVC is between 0.70 and 0.80 in normal adults; a
value less than 0.70 indicates airflow limitation and thus of COPD.
FEV
1
is influenced by the age, sex, height, and ethnicity, and is
best considered as a percentage of the predicted normal value.
There is a vast literature on normal values; those appropriate for
local populations should be used
1,2,3,4
.

24
Why do Spirometry for COPD?
? Spirometry is needed to make a clinical diagnosis of COPD.
? Together with the presence of symptoms, spirometry helps gauge
COPD severity and can be a guide to specific treatment steps.
? A normal value for spirometry effectively excludes the diagnosis of
clinically relevant COPD.
? The lower the percentage predicted FEV
1
, the worse the subsequent
prognosis.
Figure 1A: Normal Spirogram
1 2 3 4 5 6
1
2
3
4
V
ol
u
m
e
,

l
i
t
e
r
s

Time, seconds
5
1
FEV
1
= 4L
FVC = 5L
FEV
1
/FVC = 0.8
V
o
l
u
m
e
,

l
i
t
e
r
s

Time, seconds
5
4
3
2
1
1 2 3 4 5 6
FEV
1
= 1.8L
FVC = 3.2L
FEV
1
/FVC = 0.56
Obstructive
Figure 2.1B. Spirometry - Obstructive DiseaseFigure 2.1A. Spirometry - Normal Trace
Figure 1B: Spirogram Typical of Patients with Mild to Moderate COPD*
1 2 3 4 5 6
1
2
3
4
V
ol
u
m
e
,

l
i
t
e
r
s

Time, seconds
5
1
FEV
1
= 4L
FVC = 5L
FEV
1
/FVC = 0.8
V
o
l
u
m
e
,

l
i
t
e
r
s

Time, seconds
5
4
3
2
1
1 2 3 4 5 6
FEV
1
= 1.8L
FVC = 3.2L
FEV
1
/FVC = 0.56
Obstructive
Figure 2.1B. Spirometry - Obstructive DiseaseFigure 2.1A. Spirometry - Normal Trace

25
? FEV
1
declines over time and usually faster in COPD than in healthy
subjects. Spirometry can be used to monitor disease progression,
but to be reliable the intervals between measurements must be at
least 12 months.
What You Need to Perform Spirometry
Several types of spirometers are available. Relatively large bellows or
rolling-seal spirometers are usually only available in pulmonary function
laboratories. Calibration should be checked against a known volume (e.g.,
from a 3-litre syringe) on a regular basis. There are several smaller hand-
held devices, often with electronic calibration systems.
A hard copy of the volume-time plot is very useful to checkoptimal
performance and interpretation, and to exclude errors.
Most spirometers require electrical power to permit operation of the motor
and/or sensors. Some battery-operated versions are available that can
dock with a computer to provide hard copy.
It is essential to learn how your machine is calibrated and when and how
to clean it.
How to Perform Spirometry
Spirometry is best performed with the patient seated. Patients may be
anxious about performing the tests properly, and should be reassured.
Careful explanation of the test, accompanied by a demonstration, is very
useful. The patient should:
? Breathe in fully.
? Seal their lips around the mouthpiece.
? Force the air out of the chest as hard and fast as they can until their
lungs are completely “empty.”
? Breathe in again and relax.
Exhalation must continue until no more air can be exhaled, must be at least
6 seconds, and can take up to 15 seconds or more.

26
Like any test, spirometry results will only be of value if the expirations are
performed satisfactorily and consistently. Both FVC and FEV
1
should be the
largest value obtained from any of 3 technically satisfactory curves and the
FVC and FEV
1
values in these three curves should vary by no more than
5% or 150 ml, whichever is greater. The FEV
1
/FVC is calculated using the
maximum FEV
1
and FVC from technically acceptable (not necessarily the
same) curves.
Those with chest pain or frequent cough may be unable to perform a
satisfactory test and this should be noted.
Where to find more detailed information on spirometry:
1. GOLD: A spirometry guide for general practitioners and a teaching
slide set is available: http://www.goldcopd.org
2. American Thoracic Society
http://www.thoracic.org/adobe/statements/spirometry1-30.pdf
3. Australian/New Zealand Thoracic Society
http://www.nationalasthma.org.au/publications/spiro/index.htm
4. British Thoracic Society
http://www.brit-thoracic.org.uk/copd/consortium.html

MDI: metered dose inhaler inh: inhalation
DPI: dry powder inhaler act: actuation
SMI: soft mist inhaler soln: solution
ERT: extended-release tablet 

Appendix 1. COPD medications available in the United States (listing here does not indicate inclusion on the UWHC
formulary, refer to specific formulary listings for status of various agents). From Chronic Obstructive Pulmonary Disease
Clinical Practice Guideline. Revision date 5/2014; Appendix contact Philip Trapskin, PharmD, 265-0341,
PTrapskin@uwhealth.org.  
Medication Inhaler
Nebulization
Solution
Oral (Injectable
products where
noted)
Duration of
Action
Short-acting beta
2
-agonists
Albuterol Sulfate
- ProAir
®
MDI
- Proventil
®
MDI
- Ventolin
®
MDI
- Accuneb
®
nebulization
- VoSpire
®
ERT
108 mcg/act
0.63 mg/3 mL
1.25 mg/3 mL
2.5 mg/3 mL
5 mg/mL
Tablet:
2 mg, 4 mg

Oral Syrup:
2 mg/5 mL

ERT:
4 mg, 8 mg
Inhaled and oral:
4-6 hours

ERT:
12 hours
Levalbuterol
- Xopenex
®
MDI
- Xopenex
®
nebulization
45 mcg/act
0.31 mg/3 mL
0.63 mg/3 mL
1.25 mg/3 mL
1.25 mg/0.5 mL

8 hours
Terbutaline
- tablet
- injection
Tablet:
2.5 mg, 5 mg

Injection:
1 mg/mL
4-6 hours
Metaproterenol
- tablet
- syrup
Tablet:
10 mg, 20 mg

Syrup:
10 mg/5 mL
4-6 hours
Long-acting beta
2
-agonists
Arformoterol Tartrate
- Brovana
®
nebulization
15 mcg/2 mL

12 hours
Formoterol Fumarate
- Foradil Aerolizer
®
DPI
- Perforomist
®
nebulization
12 mcg/inh 20 mcg/2 mL

12 hours
Indacaterol Maleate
- Arcapta Neohaler
®
DPI
75 mcg/inh

24 hours
Salmeterol Xinafoate
- Serevent Diskus
®
DPI
50 mcg/inh

12 hours
Short-acting anticholinergics
Ipratropium Bromide
- Atrovent
®
MDI
- Atrovent
®
nebulization
17 mcg/act 0.5 mg/2.5 mL

6 hours
Long-acting anticholinergics
Aclidinium Bromide
- Tudorza Pressair
®
DPI
400 mcg/inh

12 hours
Tiotropium Bromide
- Spiriva HandiHaler
®
DPI
18 mcg/inh

24 hours
Umeclidinium Bromide
- Incruse Ellipta
®
DPI
62.5 mcg/inh 24 hours
Combination short-acting beta
2
-agonist and short-acting anticholinergic
Albuterol Sulfate/Ipratropium
Bromide
- Combivent Respimat
®
MDI
- Duoneb
®
nebulization

100/20 mcg/act 2.5/0.5 mg/3 mL

4-6 hours

MDI: metered dose inhaler inh: inhalation
DPI: dry powder inhaler act: actuation
SMI: soft mist inhaler soln: solution
ERT: extended-release tablet 
Medication Inhaler
Nebulization
Solution
Oral (Injectable
products where
noted)
Duration of
Action
Combination long-acting beta
2
-agonist and long-acting anticholinergic
Vilanterol Trifenatate
/Umeclidinium Bromide
- Anoro Ellipta
®
DPI
62.5/25 mcg/inh

24 hours
Methylxanthines
Aminophylline
- injection

Injection:
25 mg/mL
Variable, up to
24 hours
Theophylline
- Theochron
®
12-hour ERT
- 24-hour ERT
- Theo-24
®
24-hour ER capsule
- oral solution
- Elixophyllin
®
elixir
- injection

12-hour ERT:
100 mg, 200 mg,
300 mg, 450 mg

24-hour ERT:
400 mg, 600 mg

24-hour ER
capsule:
100 mg, 200 mg,
300 mg, 400 mg

Solution and
Elixir:
80 mg/15 mL

Injection:
0.8 mg/mL, 1.6
mg/mL
12-hour ERT:
12-24 hours

24-hour ERT and
capsule:
24 hours
Inhaled corticosteroids
Beclomethasone Dipropionate
- Qvar
®
MDI
40 mcg/act
80 mcg/act
12 hours
Budesonide
- Pulmicort Flexhaler
®
DPI
- Pulmicort
®
nebulization
90 mcg/inh
180 mcg/inh
0.25 mg/2 mL
0.5 mg/2 mL
1 mg/2 mL

12 hours
Ciclesonide
- Alvesco
®
MDI
80 mcg/act
160 mcg/act
12 hours
Flunisolide

- Aerospan
®
MDI
80 mcg/act 12 hours
Fluticasone Propionate
- Flovent Diskus
®
DPI
- Flovent
®
MDI
DPI:
50 mcg/inh
100 mcg/inh
250 mcg/inh

MDI:
44 mcg/act
110 mcg/act
220 mcg/act

12 hours
Mometasone Furoate
- Asmanex
®
DPI
110 mcg/inh
220 mcg/inh
12 hours
  

MDI: metered dose inhaler inh: inhalation
DPI: dry powder inhaler act: actuation
SMI: soft mist inhaler soln: solution
ERT: extended-release tablet 
Combination long-acting beta
2
-agonists and corticosteroid
Formoterol Fumarate
/Budesonide
- Symbicort
®
MDI
4.5/80 mcg/act
4.5/160 mcg/act
12 hours
Formoterol Fumarate
/Mometasone Furoate
- Dulera
®
MDI
5/100 mcg/act
5/200 mcg/act
12 hours
Salmeterol Xinafoate
/Fluticasone Propionate
- Advair Diskus
®
DPI
- Advair
®
MDI
DPI:
50/100 mcg/inh
50/250 mcg/inh
50/500 mcg/inh

MDI:
21/45 mcg/act
21/115 mcg/act
21/230 mcg/act

12 hours
Vilanterol
Trifenatate/Fluticasone Furoate
- Breo Ellipta
®
DPI
25/100 mcg/inh 24 hours
Systemic corticosteroids
Prednisone
- tablet
- Rayos
®
delayed-release tablet
- solution
- Intensol
®
concentrated solution

Tablet:
1 mg, 2.5 mg, 5
mg, 10 mg, 20
mg, 50 mg

Delayed-release
tablet:
1 mg, 2 mg, 5 mg

Solution:
5 mg/5 mL
5 mg/1 mL
12-24 hours
Methylprednisolone
- Medrol
®
tablet
- Solu-Medrol
®
injection

Tablet:
2 mg, 4 mg, 8
mg, 16 mg, 32
mg

Injection:
40 mg, 125 mg,
500 mg, 1000 mg
12-24 hours
Phosphodiesterase-4 inhibitors
Roflumilast
- Daliresp
®

500 mcg tab 24 hours