Emp Copd

EMERGENCY MEDICINE PRACTICE
A N E V I D E N C E - B A S E D A P P ROAC H T O E M E RG E N C Y M E D I C I N E
Acute Exacerbations Of COPD:

A Practical Approach
To Differential Diagnosis
And Management
11:07 p.m.: A 55-year-old woman is brought into the ED with difficulty breathing; she
is barely able to speak and has that familiar look of terror in her eyes. The medics think
that she has a history of CHF, hypertension, and asthma, as they found containers of
albuterol, lisinopril, and furosemide scattered on her kitchen table.
Barely able to speak, she gasps, Cant breathe. Her physical exam is hardly more
informative. She is diaphoretic and her lungs demonstrate poor airflow. There are
scattered rales in all fields; her legs show some mild edema. The monitor shows a sinus
tachycardia, and a quick chest film demonstrates a vertical heart with questionable
perihilar fullness.
The nurses urge you on: How much oxygen do you want? Should we give some
Lasix, draw some cardiac enzymes? How about some steroids, albuterol, or a nitroglycerin drip? Do you want the airway cart?
Decision time.
Critical Appraisal Of The Literature
Guidelines
There are several guidelines that address the diagnosis and management of
chronic obstructive pulmonary disease (COPD). Influential guidelines published in the mid-1990s include those by the American Thoracic Society,1 the
European Respiratory Society,2 and the British Thoracic Society.3 More recent is
the Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop
Summary (also available online at http://www.goldcopd.com).4 It represents a
combined effort of the World Health Organization and the National, Heart,
Lung, and Blood Institute of the National Institutes of Health. This guideline is
Stephen A. Colucciello, MD, FACEP,

Assistant Chair, Department of
Emergency Medicine, Carolinas
Medical Center, Charlotte, NC;
Associate Clinical Professor,
Department of Emergency
Medicine, University of North
Carolina at Chapel Hill, Chapel
Hill, NC.
Associate Editor
Andy Jagoda, MD, FACEP, Professor
of Emergency Medicine; Director,
International Studies Program,
Mount Sinai School of Medicine,
New York, NY.
Editorial Board
Judith C. Brillman, MD, Residency
Director, Associate Professor,
Medicine, The University of
New Mexico Health Sciences
Center School of Medicine,

Albuquerque, NM.
W. Richard Bukata, MD, Assistant
Clinical Professor, Emergency
Medicine, Los Angeles County/
USC Medical Center, Los Angeles,
CA; Medical Director, Emergency
Department, San Gabriel Valley
Medical Center, San Gabriel, CA.
Francis M. Fesmire, MD, FACEP,
Director, Chest PainStroke
Center, Erlanger Medical Center;
Assistant Professor of Medicine,
UT College of Medicine,
Chattanooga, TN.
Valerio Gai, MD, Professor and Chair,
Medicine, University of Turin, Italy.
Michael J. Gerardi, MD, FACEP,
Clinical Assistant Professor,
Medicine, University of Medicine
and Dentistry of New Jersey;
Director, Pediatric Emergency
Medicine, Childrens Medical
Center, Atlantic Health System;
Vice-Chairman, Department of
Authors
Mary T. Ryan, MD
Attending Physician, Department of Emergency
Medicine, Lincoln Medical and Mental Health Center,
Bronx, NY; Clinical Instructor in Emergency Medicine,
Weill College of Medicine, Cornell University, New
York, NY.
Michael S. Radeos, MD, MPH
Attending Physician, Department of Emergency
Medicine, Lincoln Medical and Mental Health Center,
Bronx, NY; Assistant Professor in Emergency Medicine,
Weill College of Medicine, Cornell University, New
York, NY.
Peer Reviewers
Rita K. Cydulka, MD, MS
Associate Professor, Case Western Reserve University;
Faculty, MetroHealth Medical Center Emergency
Medicine Residency, Cleveland, OH.
David Della-Giustina, MD
Program Director, MadiganUniversity of Washington
Emergency Medicine Residency, Tacoma, WA.
CME Objectives
Statistics are like a bikini: what they reveal is suggestive,

but what they conceal is vital.Aaron Levenstein
Editor-in-Chief
April 2002
Volume 4, Number 4
Emergency Medicine, Morristown

Memorial Hospital.
Michael A. Gibbs, MD, FACEP,
Residency Program Director;
Medical Director, MedCenter Air,
Medicine, Carolinas Medical
Center; Associate Professor of
Emergency Medicine, University
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Gregory L. Henry, MD, FACEP,
CEO, Medical Practice Risk
Assessment, Inc., Ann Arbor,
MI; Clinical Professor, Department
of Emergency Medicine, University
of Michigan Medical School, Ann
Arbor, MI; President, American
Physicians Assurance Society, Ltd.,
Bridgetown, Barbados, West Indies;
Past President, ACEP.
Jerome R. Hoffman, MA, MD, FACEP,
Professor of Medicine/Emergency
Medicine, UCLA School of
Medicine; Attending Physician,
UCLA Emergency Medicine Center;
Upon completing this article, you should be able to:

1. safely manage the acutely ill patient with COPD in the
ED, using an evidence-based approach;
2. list different treatment options and explain the
rationale for their use;
3. formulate a differential diagnosis for a patient with an
acute exacerbation of COPD; and
4. explain and avoid some common pitfalls in the
management of COPD.
Date of original release: April 1, 2002.

Date of most recent review: March 15, 2002.
See Physician CME Information on back page.
Co-Director, The Doctoring
Program, UCLA School of Medicine,
Los Angeles, CA.
John A. Marx, MD, Chair and Chief,
Medicine, Carolinas Medical
Center, Charlotte, NC; Clinical
Professor, Department of
of North Carolina at Chapel Hill,
Chapel Hill, NC.
Michael S. Radeos, MD, MPH,
Attending Physician, Department
of Emergency Medicine,
Lincoln Medical and Mental
Health Center, Bronx, NY;
Assistant Professor in Emergency
Medicine, Weill College of
Medicine, Cornell University,
New York, NY.
Steven G. Rothrock, MD, FACEP, FAAP,
Associate Professor
of Emergency Medicine, University
of Florida; Orlando Regional
Medical Center; Medical Director of
Orange County Emergency
Medical Service, Orlando, FL.

Alfred Sacchetti, MD, FACEP,
Research Director, Our Lady of
Lourdes Medical Center, Camden,
NJ; Assistant Clinical Professor
of Emergency Medicine,
Thomas Jefferson University,
Philadelphia, PA.
Corey M. Slovis, MD, FACP, FACEP,
Professor of Emergency Medicine
and Chairman, Department of
Emergency Medicine, Vanderbilt
University Medical Center;
Medical Director, Metro Nashville
EMS, Nashville, TN.
Mark Smith, MD, Chairman,
Medicine, Washington Hospital
Center, Washington, DC.
Charles Stewart, MD, FACEP,
Colorado Springs, CO.
Thomas E. Terndrup, MD, Professor
and Chair, Department of
of Alabama at Birmingham,
Birmingham, AL.
of the airspace distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious
fibrosis.1 Chronic bronchitis is defined as the presence of
chronic productive cough for three months in each of two
successive years in a patient in whom other causes of
chronic cough have been excluded. However, McCrory et
al admit that in fact, separating these entities is difficult
both when evaluating clinical studies and when practicing
clinical medicine.
GOLD updates the definition of COPD as a disease
state characterized by airflow limitation that is not fully
reversible. (See Table 1.) The airflow limitation is usually
both progressive and associated with an inflammatory
response of the lungs to noxious particles or gases. While
these various definitions are a necessary irritation, the
emergency physician should consider COPD in any patient
with cough, sputum production, or dyspnea.
mostly directed toward the primary care provider and is

less geared toward emergency management.
The American College of PhysiciansAmerican Society
of Internal Medicine and the American College of Chest
Physicians have published a competing guideline. This
evidence-based clinical practice guideline is entitled
Evidence base for management of acute exacerbations of
chronic obstructive pulmonary disease.5 (These recommendations are hereafter referred to as the Joint Guidelines.)
The Feds have entered the fray with a sponsored
guideline. This one, endorsed by the Agency for Healthcare
Research and Quality, involves an evidence-based article
published by researchers from Duke University and
Memorial Sloan-Kettering Cancer Center (hereafter referred
to as the McCrory guidelines).6 In this article, the authors
rate various therapeutic interventions, diagnostic tests and
risk stratification based on the existing literature. Unlike the
Cochrane Collaboration, this group did not perform metaanalyses of the pooled data. This comprehensive summary
is available at the Agency for Healthcare Research and
Quality Web site (http://www.ahcpr.gov/clinic/epcsums/
copdsum.htm).6
Diagnostic Uncertainty
Beyond the confusion associated with the evolving definition of COPD, there is evidence to suggest that physicians
are not very good at diagnosing this diseaseeven when
the presentation is relatively straightforward. In one study,
the authors presented a clinical scenario to 75 primary care
providers in Canada and asked them to provide a diagnosis.7 The case involved a 52-year-old smoker with recurrent
respiratory infections and wheeze. Half of the primary care
physicians were told that the patient had history of chronic
bronchitis, while the other half were not. The physicians
who were given a history of chronic bronchitis diagnosed
COPD twice as often as those who were not told this fact. A
more recent study presented a similar scenario to primary
care providers in the U.S. and Canada.8 This time, they
randomized primary care physicians so that half received
the scenario with the patient as a male, while the other half
were given the identical scenario with the patient as a
female. They found that 65% of the physicians diagnosed
COPD in the male patient, while only 49% diagnosed the
woman with COPD (P < 0.05). Systematic under-diagnosing
of women with COPD may also occur in the ED.9
Definitions
The McCrory article and the older guidelines separate
COPD into chronic bronchitis, emphysema, and asthma,
while the GOLD guidelines do not. This distinction is
problematic because emphysema is defined anatomically,
while chronic bronchitis is determined by clinical criteria.
According to the American Thoracic Society Guidelines,
emphysema is an abnormal permanent enlargement
Table 1. GOLD Classification Of COPD By Severity.

Stage
0: At Risk
Characteristics
Normal spirometry
Chronic symptoms (cough, sputum
production)
I: Mild COPD
FEV1/FVC < 70%

FEV1 80% predicted
With or without chronic symptoms
(cough, sputum production)
II: Moderate COPD
FEV1/FVC < 70%

30% FEV1 < 80% predicted
(IIA: 50% FEV1 < 80% predicted)
(IIB: 30% FEV1 < 50% predicted)
III: Severe COPD
FEV1/FVC < 70%

FEV1 < 30% predicted, or the
presence of respiratory failure,* or
clinical signs of right heart failure
Epidemiology
In 1990, the World Health Organization reported the
prevalence of COPD to be 9.34/1000 in men and 7.33/1000
in women. The exact prevalence of COPD in the U.S. is
unknown, but it is estimated that approximately 14 million
Americans suffer from this condition.10 (This number is
likely an underestimate, since COPD remains underdiagnosed in the primary care setting.11) While data on ED
visits for COPD are difficult to find, data on COPD discharges are easily available.12 In 1998, nearly 700,000 people
were discharged from the hospital with a diagnosis of
COPD. The rate of women discharged for COPD exceeded
men in 1992, and the ratio of women to men has been
increasing yearly since then. There is clear evidence that the
prevalence of COPD has doubled in the past few decades in
women while remaining relatively stable in men.13 This may
reflect a combination of increased prevalence of smoking
* Respiratory failure: PaO2 < 8.0 kPa (60 mmHg) with or

without PaCO2 > 6.7 kPa (50 mmHg) while breathing air at
sea level.
Used with permission from: Pauwels RA, Buist AS, Ma P, et al. Global
strategy for the diagnosis, management, and prevention of chronic
obstructive pulmonary disease: National Heart, Lung, and Blood
Institute and World Health Organization Global Initiative for Chronic
Obstructive Lung Disease (GOLD): executive summary. Respir Care
2001 Aug;46(8):798-825.
Emergency Medicine Practice
April 2002
parenchyma, leading to loss of lung elasticity. Once the

damage has occurred, it is quite refractory to treatment. This
underscores the importance of preventive treatmentmost
notably, smoking cessation. Current pharmacotherapy has
little effect on disease progression.10,16
Macrophages, neutrophils, and CD8+ T lymphocytes
accelerate parenchymal injury due to tobacco smoke.
(This is in contrast to asthma, in which CD4+ lymphocytes
and eosinophils are the predominant cell types.) In
COPD, tobacco smoke leads to loss of surfactant, increase
in goblet cells, and cellular activation. Enzymes released
from macrophages and neutrophils (such as neutrophil
elastase, cathepsins, and matrix metalloproteinases)
damage the distal airways, leading to premature airway
collapse on exhalation.
among women as well as the fact that women may be more

susceptible to the effects of tobacco smoke.14
COPD is currently the fourth leading cause of death in
the world, and the only cause of death that is still increasing.
Among industrialized countries, the U.S. ranks high in
COPD mortality (sixth for women and ninth for men).13
Morbidity of COPD increases with age and is greater in men
than in women. In 2000, total costs (direct and indirect) of
COPD in the U.S. reached $30.4 billion.4 Direct costs related
to ED visits are estimated at $148 million.15
You and I both know that Twinkies dont kill people....
The difference between cigarettes and Twinkies...is death.
The tobacco industry should know: When it comes to Twinkies,
Id rather fight than quit.Henry Waxman (b. 1939),
U.S. Democratic congressman from California.
Los Angeles Times, p. E2 (June 9, 1994)
Differential Diagnosis
Etiology
In the ED, it is important to distinguish between mimics of

COPD and co-existing illness in conjunction with COPD.
Many patients with chronic lung disease have coexisting
medical problems, such as pulmonary embolism (PE),
congestive heart failure (CHF), volume overload, pneumothorax, and pneumonia.
In industrialized countries, smoking is the leading cause of

COPD. While tobacco smoke is a key risk factor for development of COPD, only 15% of smokers develop COPD.
Conversely, 10% of those with COPD have no smoking
history.16,17 In addition to smoking, the risk of developing
COPD involves host factors, environmental exposures, and
a combination of both. The major host risk factor is 1antitrypsin (1-AT) deficiency.
The major environmental exposures include tobacco
smoke, heavy exposure to occupational dust and chemicals
(vapors, irritants, and fumes), and indoor/outdoor air
pollution. One population-based study demonstrated that
chronic exposure to dust, fumes, or gases increased the odds
of obstructive pulmonary disease even after controlling for
cigarette smoking.18
There is evidence that passive smoking also increases
the risk of COPD. The SAPALDIA study (Swiss Study on
Air Pollution and Lung Disease in Adults) on passive
smoking found a dose-dependent increase with hours per
day of exposure for dyspnea, wheeze, and asthma. The
association with bronchitis was more strongly related to the
number of years of exposure.19
Asthma
While there are differences between asthma and COPD, it is
important to realize that about 10% of those with COPD
may also have clinical features of asthma. This subgroup is
also referred to as wheezy bronchitis (see Figure 1) and
should be treated as asthma.20 Because it is difficult to
identify this entity based on the ED history and physical
exam, patients with evidence of bronchospasm should be
treated as if they have a reversible condition.
Congestive Heart Failure

It is possible to distinguish between acute exacerbations of
COPD and CHF based on the history, physical exam, and
simple bedside maneuvers. Even the words that patients
use to describe their dyspnea may be helpful. In one study,
53 patients with seven types of breathing problems were
asked to characterize their dyspnea.21 Patients with COPD
used work or hunger, while those with CHF used
rapid, suffocating, and hunger. The only descriptor
associated with pulmonary embolism was rapid. (While
other studies have found similar results,22,23 language alone
Pathophysiology
The hallmarks of COPD include chronic airflow obstruction
of the small airways and enzymatic destruction of the lung
Figure 1. Overlap between asthma and COPD. Approximately 10% of patients with COPD also have asthma and
therefore share pathologic features.
~10%
COPD
Neutrophils
Mild to no airway hyperreactivity
Mild to no bronchodilator response
Mild to no corticosteroid response
Generally begins in adulthood
Asthma
Eosinophils
Airway hyperreactivity
Bronchodilator response
Corticosteroid response
Generally begins in childhood
Often associated with atopy
Wheezy bronchitis
Used with permission from: Barnes PJ. Mechanisms in COPD. Differences from asthma. Chest 2000;117:10S-14S.
April 2002
should not be used to exclude a dangerous condition.) (See

also the August 1999 issue of Emergency Medicine Practice,
Dyspnea: Fear, Loathing And Physiology.)
Mulrow et al reviewed the literature on how well the
history and physical examination predict various causes of
dyspnea, including CHF and COPD.24 They found that
orthopnea (likelihood ratio, 2.0) and dyspnea with exertion
(likelihood ratio, 1.3) were both associated with CHF. Other
clinical factors, such as cough, smoking, wheezing, and
edema, were less valuable. Regarding physical maneuvers,
the abdominal jugular reflux appears to be strongly
associated with CHF. To perform this test, the patient is
placed supine with the head of the bed at 45, and the
physician presses on the upper abdomen for 10 seconds. A
positive study shows a rise in jugular venous pulsations of
at least 3 cm over baseline.
Chest radiography may not always distinguish
between causes of respiratory distress. Those patients with
chronic lung disease who develop acute CHF often do not
have typical findings such as cardiomegaly or bat wing
infiltrates. This is especially true in the case of acute
diastolic dysfunction.25
Spirometry may help distinguish acute exacerbations of
COPD from CHF. In one study of 40 patients presenting
with acute dyspnea, the peak expiratory flow rate (PEFR)
overlapped between groups. However, a cutoff value of 150
L/min was 82% predictive for CHF, while a level below 150
L/min gave a positive predictive value (PPV) of 83% for
pulmonary causes of dypnea.26
B-natruretic peptide (BNP) may be one of the best ways to
distinguish COPD from CHF in the ED. In one study, the BNP
measurement was more accurate than any other single
variablewhether history, physical, chest x-ray, or ECGin
determining the presence of heart failure.27 (See also the
February 2002 issue of Emergency Medicine Practice, Acutely
Decompensated Heart Failure: Diagnostic And Therapeutic
Strategies For The New Millennium.)
include advanced age, recent trauma or surgery, prior

thromboembolic disease, cancer, heart failure, systemic
lupus, and arteriopathy.28-30 While many patients with PE
complain of pleuritic chest pain, at least a third have
painless dyspnea. Arterial blood gas (ABG) results cannot
distinguish between PE and COPD.31 Fortunately, there are
other means that identify the patient with PE.32,33
The combination of a whole-blood d-dimer assay and
alveolar dead-space volume can rule out PE in the low-risk
patient.32 In one study of 64 subjects with PE, 63 had either
an abnormal d-dimer, an abnormal dead-space, or both
(sensitivity, 98.4%; 95% CI, 91.6%-100%). Another approach
to excluding PE in patients with known COPD involves a
combination of d-dimer, lower-extremity Doppler, V/Q
scans, and spiral CT angiography. In one multicenter study,
the authors state that the diagnosis of PE is not affected
by the presence of COPD when clinicians follow a
rigorous algorithm.33
Acute Coronary Syndrome

Shortness of breath may be the major (or only) complaint
in patients with acute coronary syndrome (ACS). In one
large study, a chief complaint of dyspnea was associated
with a likelihood ratio of 2.7 (95% CI, 1.1-6.5) for missed
diagnosis of ACS.34 The emergency physician should
obtain an electrocardiogram and cardiac enzymes
whenever ACS is likely. However, the literature provides
little direction as to when we should suspect ACS in a
patient with possible COPD. Clinical clues may include a
prior history of coronary artery disease, significant cardiac
risk factors, ischemic-type pain (neck, chest, arms, back,
or upper abdomen), unexplained diaphoresis, and newonset dyspnea.
Pneumothorax
COPD is a known risk factor for a secondary pneumothorax, particularly when emphysema produces pleural blebs.
Clinical clues may include asymmetrical chest expansion or
breath sounds and, in the case of tension pneumothorax,
hypotension or tracheal deviation. However, small pneumothoraces can easily be missed on clinical exam yet still
produce acute decompensation. Patients on positive
pressure ventilation are at increased risk of developing a
tension pneumothorax.
A chest x-ray is generally adequate to make the
diagnosis, and expiratory films can be helpful in detecting
small pneumothoraces.35
Pulmonary Embolism
The emergency physician must consider PE in any patient
with acute dyspnea. In general, clinical risk factors for PE
Key Points In COPD

1. COPD and asthma may co-exist in approximately 10% of
patients (wheezy bronchitis).
2. Women are more likely than men to go undiagnosed with
COPD despite meeting diagnostic criteria.
3. Noninvasive ventilation has been shown to prevent
tracheal intubation in patients with moderate-to-severe
acute exacerbations of COPD.
4. The differential diagnosis for patients with acute
exacerbations of COPD is extensive. It includes lifethreatening conditions such as pulmonary embolism,
congestive heart failure, myocardial infarction, pneumonia,
and tension pneumothorax.
5. Advise all patients with COPD to quit smokingthis is the
most important treatment for patients with COPD.
Pneumonia
Fever is an important clue to the diagnosis of pneumonia.
Consider obtaining a rectal temperature in patients who
present with a normal oral temperature but who appear
sicker or are hot to the touch. Two ED studies have found
that oral temperatures may be falsely normal in patients
with tachypnea and/or mouth breathing.36,37 However, the
chest film is the best ED screening test for pneumonia.
Lobar Atelectasis
Lobar atelectasis is another important consideration in the
April 2002
167 patients with no prior history of COPD who presented

to a VA clinic for medical clearance.41 The key clinical
elements, derived from a logistic regression model, were the
number of years smoked, patient report of wheezing, and
wheezing on auscultation.
dyspneic patient, especially in those with a history of

COPD. Excessive secretions combined with impaired
cough contribute to this condition; a mucous plug may
lead to collapse of all or part of a lung. Physical examination
may show asymmetrical expansion and unilateral decrease
in breath sounds, but findings are often subtle or indeterminate. Chest x-ray will typically demonstrate loss of lung
volume and elevation of the hemidiaphragm on the
affected side.
History
History Of Present Illness And Review Of Systems
Determine the presence of fever, changes in sputum
production, hemoptysis, and whether or not the patient has
chest pain. Other important questions may include whether
the patient experiences orthopnea and changes in exercise
tolerance. Ascertain the acuity of onset and how rapidly the
patient is deteriorating. If the deterioration is very acute,
consider PE, ACS, CHF, and pneumothorax in the differential diagnosis.
It is tempting to assume that shortness of breath
in a patient with a history of COPD reflects an acute
exacerbation of the disease. This may not be so, especially if
the patient complains of atypical symptoms. Some associated symptoms may be especially revealing, such as the
unilateral leg swelling that may occur with deep venous
thrombosis (DVT).
Establish the patients baseline status. This is
important in ascertaining how acutely ill the patient is and
will help determine the need for hospital admission or
discharge. It may also provide indirect information about
how well the patients disease is controlled on the current
medication regimen or if noncompliance is a factor. The
following questions may be helpful:
When was your last ED visit?
Have you ever been admitted? When was the
last admission?
Have you ever been intubated?
Do you have oxygen at home? How many hours
a day do you need it?
How bad is this attack?
Prehospital Care
The priority of prehospital care in acute exacerbations of
COPD is to ensure maintenance of the airway. If the patient
is obtunded or unable to ventilate effectively, assisted
ventilation (usually by tracheal intubation) is essential.
Although there are airway adjunctslaryngeal mask
airway and the Combitubethat may provide temporizing
measures in a difficult, non-obstructed airway, they may not
allow effective ventilation due to high airway pressures.
These interventions may result in gastric insufflation instead
of proper ventilation. Pulse oximetry may be helpful in
patients who show signs of respiratory distress or altered
mental status.
Clinical trials demonstrate that the prehospital administration of either aerosolized albuterol or subcutaneous
terbutaline significantly reduces respiratory distress in
patients with bronchospasm.38,39 While aerosolized
ipratropium is not well-studied in the prehospital setting,
there is no apparent reason why it would be any less
effective in the ambulance than in the ED.
Studies on the prehospital use of noninvasive ventilation (NIV), such as CPAP or BiPAP, are limited; most trials
involve CHF rather than COPD. One study examining the
utility of BiPAP in the field found it to be safe and easy to
use. Although the pre- and post-treatment oxygen saturation levels were greater for the BiPAP group (13.71% vs
6.69%) than the control group, no statistical differences were
noted between the groups for mortality, intubation rate, or
length of hospital stay.40 (However, note that the patients
studied were those believed to have an exacerbation of
CHF, not COPD. Further, the outcome measure was a
change in SaO2.)
I have every sympathy with the American who was

so horrified by what he had read about the effects of smoking
that he gave up reading.Henry G. Straus
Medication History
Changes in medication regimens or doses, either intentional
or accidental, may cause patients with COPD to deteriorate.
Find out whether the patient uses an inhaler. Is the patient
currently taking steroids; if not, when was he or she last on
steroids? For patients on home oxygen, determine how
many liters per minute they use. Specifically ask if they
take a theophylline preparation (such as Uniphyl,
Theo-Dur, or Theolair).
If noncompliance seems to be an important contributing factor, attempt to establish why it has occurred and
address practical difficulties the patient may face. Manipulation and coordination of metered-dose inhalers (MDIs) may
be difficult. Sending a patient home without addressing
these issues invites an ED relapse.42 Some patients may be
reluctant to admit noncompliance to the physician. Nonconfrontational questions may include: Have you run out
of your medication? How do you take your medication?
Always take an emergency leisurely.Chinese proverb
Emergency Department Evaluation

As with many conditions seen in the ED, the evaluation and
stabilization of the acutely ill patient with COPD may occur
in tandem. If the patient is not able to communicate due to
the severity of the exacerbation, ask the medics and family
members to provide the history. If the patient is moribund,
quickly determine the patients code status and ask about a
living will or advance directives. Never withhold life-saving
airway intervention in a patient whose advance directive
cannot be verified beyond a reasonable doubt.
When a patient presents with acute dyspnea but no
prior history of obstructive airway disease, certain elements
of the history, physical, and bedside diagnostics may
suggest the diagnosis. In one study, researchers evaluated
April 2002
chest (no wheezes or rales in the presence of respiratory

distress) is worrisome and may herald respiratory failure.
Do you ever forget to take your medications? Show me

how you use your inhaler/spacer. How do you get to the
pharmacy or clinic?
Polypharmacy or drug-drug interactions are important
factors to consider. Many drugs can directly or indirectly
produce bronchospasm in certain individuals. Implicated
medications include -blockers, aspirin, nonsteroidal antiinflammatory drugs, cholinergics, and prostaglandin
inhibitors. Some patients with COPD may develop respiratory depression with small doses of sedating drugs. Alcohol
is a frequent culprit.43 Remember to ask patients about any
over-the-counter or herbal preparations they may be taking,
as these may also interact with their prescribed medications.
Circulation
Determine whether the patient is in overt shock by palpating peripheral pulses and evaluating the skin color and
temperature. If the patient has signs of hemodynamic
compromise, consider tension pneumothorax, cardiogenic
shock, theophylline toxicity, dehydration, or sepsis.
The cardiac exam may provide clues to CHF, such as a
gallop rhythm. Edema of the extremities can occur in many
conditions (including advanced COPD in association with
pulmonary hypertension), but unilateral leg swelling should
raise concern for DVT and PE. A positive hepatojugular
reflux provides strong evidence for CHF.
Past Medical History

The patient or his family may be able to give information
about medical problems such as DVT, PE, or coronary artery
disease. Other important comorbid conditions include any
immune suppression, CHF, or renal insufficiency. Determine
whether the patient has a history of pneumothorax, prior
intubations, or ICU admissions.
Patient Monitoring
ECG Monitoring
There is little evidence to recommend routine ECG
monitoring in the patient with an acute exacerbation of
COPD. However, in most EDs, patients in distress and
those with unclear reasons for decompensation are placed
on monitors. Monitoring is also useful in patients suspected
of dysrhythmias.
Physical Examination
Quickly assess the patients distress upon entering the room.
Is he or she anxious or lethargic? Is he or she diaphoretic,
cyanotic, or in extremis? An ABCs approach may help.
Pulse Oximetry
Pulse oximetry allows for continuous noninvasive monitoring of oxygenation and is an important adjunct in the care of
a patient with an acute exacerbation of COPD.45 While
values less than 92% are worrisome, some patients with
COPD are chronically hypoxic. A review of the patients
medical record may provide a useful comparison value.
While pulse oximetry is of value in monitoring
oxygenation, it has important limitations. Of particular
concern in COPD is the fact that it gives no indication of
how well the patient is ventilating. Significant hypercarbia
can remain undetected.
Airway
Determine whether the patient has a patent airway. If not, it
is likely that the patient will need emergent endotracheal
intubation. Suction secretions as needed.
Breathing
This is the most important aspect of the physical examination in the patient with respiratory distress. Assess the
respiratory rate and effort. Tachypnea is a common finding
in acute exacerbations of COPD. Bradypnea is ominous, and
assisted ventilation should be strongly considered. Note the
use of accessory muscles, pursed lips, intercostal retractions,
and if the patient is sitting in a tripod position (leaning
forward with extended arms on knees)all are signs of
respiratory distress. Patients who are unable to converse, or
those who speak only in short sentences, are in trouble.
Assess the patients mental status; lethargy may occur with
hypoxia, hypercarbia, or both.
Next, determine whether the trachea is midline, and
observe the neck veins. Tracheal deviation is a late finding
of tension pneumothorax. If the neck veins distend during
inspiration (Kussmauls sign), the patient has a significant
increase in right-sided venous pressurepossibly due to
right ventricular infarction, tension pneumothorax, pulmonary embolism, or pericardial tamponade.44
Observe the chest wall movement. An asymmetrical
chest rise may occur with pneumothorax. During chest
auscultation, assess for symmetrical breath sounds. Asymmetry may be due to a wide variety of pathologies, including pneumothorax, atelectasis, pneumonia, effusion, or
splinting. Wheezes and rales may occur with COPD or with
CHF, foreign bodies, or interstitial lung disease. A silent
Capnometry
Some authorities believe that dynamic capnometry may
help in assessing CO2 retention and provide useful information regarding the severity of airway obstruction. However,
while the association between capnometry values and
airflow obstruction has been studied in asthma,46 its utility
in acute exacerbations of COPD is not well-established.
IV Line
Patients with mild acute exacerbations of COPD may not
need IV access. However, patients who present with severe
acute exacerbations of COPD should have at least one
reliable IV line through which parenteral medications may
be given, especially if the need for rapid sequence intubation is likely.
Diagnostic Studies
Spirometry
According to the joint guidelines by American College of
PhysiciansAmerican Society of Internal Medicine and the
American College of Chest Physicians, acute spirometry
April 2002
equally concerning as it may signal impending respiratory

and circulatory failure. Many patients with COPD will have
a baseline compensated acidosis (normal pH, elevated
PaCO2). Comparison of current to prior ABG results can be
very useful.
ABGs are often obtained to identify PE, but recent
evidence suggests that they may be no more accurate for
this purpose than the flip of a coin. In one study, researchers
prospectively evaluated consecutive patients suspected of
having PE, and compared those with and without PE. The
study showed that the ABG did not change pretest probabilities enough to alter the diagnostic work-up.50
should not be used to diagnose an acute exacerbation of COPD or

to assess its severity. A study performed in 70 ED patients
showed that FEV1 at presentation was weakly (but statistically significantly) correlated with both PCO2 and pH but
not with arterial PO2.47 These results differ from those in
patients with asthma, in which case there is a strong
correlation between spirometry and ABG values.
Spirometry may be useful in the primary care setting,
when the diagnosis of COPD is being established.4 The
GOLD authors note that it is difficult for patients with acute
exacerbations of COPD to perform spirometry, but, if they
do, then in general, PEF less than 100 L/min or FEV1 less
than 1.0 L indicates a severe exacerbation. The presence of a
post-bronchodilator FEV1 of less than 80% of the predicted
value in combination with an FEV1/FVC less than 70%
confirms the presence of airflow limitation that is not fully
reversible.4 Spirometry may also be useful when the
physician is trying to distinguish between cardiac and
pulmonary causes of dyspnea.
If spirometry is performed in the EDand it is not
recommended as a routine interventionthen physicians
should be aware of its limitations. In one ED study, the
authors found that although PEFR can measure airway
obstruction, there may be clinically significant discrepancies
between PEFR and FEV1. The study concluded that measurement of the FEV1 is preferred over PEFR because it
allows comparison with baseline studies and adheres to
previously published guidelines.48
Other Blood Tests

There are no good data to support routine blood tests in
acute exacerbations of COPD. Clinical circumstances
usually dictate when laboratory testing is indicated. An
aminophylline serum level may be useful if the patient has
been taking theophylline at home (especially if there is
nausea, tremor, or tachycardia), and cardiac enzymes are
indicated when ACS is suspected.
A chemistry panel may reveal hypokalemia in patients
taking diuretics or certain antihypertensive agents, and in
those who complain of vomiting, weakness, or palpitations.
Patients with concomitant renal failure will almost certainly
have significant electrolyte abnormalities. A number of
laboratory abnormalities are expected in patients with
advanced stages of COPD. For instance, patients with
chronic hypercapnia will demonstrate an elevated bicarbonate level.
In general, the white blood cell (WBC) count does
not provide useful management information. A high
leukocyte count does not necessarily indicate infection;
the WBC count will increase with physiologic stress, steroid
use, or -agonists.51 The complete blood count (CBC) is
useful to evaluate for polycythemia or anemia in the
appropriate clinical circumstances. D-dimer assays are
best used in the context of a verified diagnostic algorithm.31,33,52,53 Older latex agglutination assays are so
non-specific as to be almost worthless.54-56
Arterial Blood Gas

Unlike pulse oximetry or capnography, ABG values are
direct measurements of pH, PaO2, and PaCO2. From a
clinical standpoint, ABGs are most useful in patients who
have altered mental status, are in severe distress, and in
those suspected of acidosis. Other indications include
persistent hyperventilation and intractable hypoxia.
McCrory et al found indirect evidence supporting the
clinical utility of ABG. In their review, the blood gas was
occasionally helpful in gauging the severity of an exacerbation, identifying the need of oxygen therapy, and determining who might require intubation.49 The GOLD report
suggests that an ABG should be considered in all patients
with FEV1 less than 40% predicted or in those with clinical
signs suggestive of respiratory failure or right heart failure
(such as central cyanosis, ankle swelling, and an increase in
the jugular venous pressure).4 The GOLD authors give no
references for this recommendation.
The reason given for performing an ABG is to determine the severity of the exacerbation and to identify those in
need of oxygen therapy or mechanical ventilation (i.e., pH
< 7.30). While numerous and varied numbers are quoted to
quantify the need for intubation, most experienced physicians believe that the need for intubation is a clinical
determination, not one made solely using blood gas results.
A significant part of this clinical determination depends on
the patients response to therapy. This said, the finding of
acidosis is of concern in acute exacerbations of COPD. A
respiratory acidemia represents hypoventilation and
decompensation from their baseline. A metabolic acidosis is
April 2002
Brain Natriuretic Peptide

Brain natriuretic peptide (BNP) is a promising new blood
test that appears to discriminate between CHF and acute
exacerbations of COPD. Unlike the atrial natriuretic peptide,
BNP is produced primarily from the ventricles in apparent
response to ventricular wall stress.57 Davis et al studied 52
patients with acute dyspnea. Patients with CHF had
significantly higher BNP levels than patients with acute
exacerbations of COPD. These differences remained posttreatment.58 Cabanes et al also demonstrated that the BNP
was useful in differentiating acute exacerbations of COPD
from CHF.59 They studied BNP and echocardiography in 26
dyspneic patients with New York Heart Association III and
normal LV function, 17 patients with COPD, and nine
patients with unequivocal diastolic failure. BNP levels were
significantly lower in patients with acute exacerbations of
COPD compared with patients with diastolic heart failure
(14 12 pg/mL vs 224 240 pg/mL; P < 0.0001).
Treatment
Sputum Analysis
In the past, sputum induction and evaluation was common
practice. However, both the safety and value of sputum
induction are in question. Grams stains correlate poorly
with cultures.60 Sputum induction with hypertonic saline
has been associated with worsening bronchoconstriction in
patients with COPD.61
While microscopic evaluation of sputum is unnecessary, visual inspection of a patients sputum, while unappealing, is useful. Stockley et al recently noted that sputum
color may have clinical significance.62 They found that the
presence of green/purulent sputum was 94.4% sensitive
and 77.0% specific for a high-yield bacterial load. Other
studies suggest that a visual screen (or historical report) of
purulent sputums may identify those patients most likely to
benefit from antibiotic therapy.63
Oxygen Therapy
Supplemental oxygen is an essential part of ED therapy for
acute exacerbations of COPD. Administer oxygen to all
patients with acute exacerbations of COPD who present in
respiratory distress or have room air oxygen saturation
below 90%-92%.
A variety of delivery systems are available, including
nasal cannula and non-rebreather or Venturi masks.
Regardless of the mode of delivery, therapy should deliver
enough oxygen to support vital organ function (PaO2 60
mmHg, or SaO2 90%).4
This cutoff of 90% appears to be a consensus of existing
guidelines4 as well as recent clinical trials of oxygen therapy
in acute exacerbations of COPD.71 Agusti et al performed a
randomized, crossover controlled trial of supplemental
oxygen in 18 patients presenting with acute exacerbations of
COPD. They found that while Venturi masks were slightly
better than nasal prongs at maintaining SaO2 of 90% or
greater, neither route worsened respiratory acidosis.71
This slight advantage of the Venturi mask may be more
than offset by patient discomfort (i.e., inability to tolerate
the mask).
In the patient with normal physiology, elevations of
CO2 are responsible for the respiratory drive. Many patients
with advanced COPD lack this physiologic prompt and
depend on hypoxia for their respiratory stimulus. If too
much oxygen is given, some patients will develop hypercapnia. The risk of this going undetected in a closely
monitored setting appears to be small.72 When acute distress
arises, provide necessary oxygen to maintain the pulse
oximeter at 90% or greater. As the patients clinical condition
improves, the concentration of oxygen can be reduced.
Chest X-Ray
Tsai et al studied guidelines for the selective ordering of
chest x-rays in patients admitted for obstructive airway
disease.64 They recommended obtaining a chest x-ray for
any patient with complicated COPD. Complicated was
defined as fever, significant distress, heart disease, IV drug
abuse, seizures, immunosuppression, other pulmonary
disease, or prior thoracic surgery.
Emerman and Cydulka recommend a more liberal
approach. They argue that the emergency physician
consider a chest x-ray for all patients presenting with COPD,
as clinical criteria in their study were unable to accurately
predict patients with a positive radiograph.65 A chest x-ray
may offer early clues to other important diagnoses, such as
pneumonia, CHF, pleural effusion, aortic dissection, and
pneumothorax.4,66
Electrocardiogram
Inhaled Therapy
-agonists And Anticholinergics
The electrocardiogram (ECG) is most useful in evaluating

patients with suspected coronary syndromes. Patients with
COPD may demonstrate a pulmonary disease pattern
with evidence of right heart strain, right axis deviation,
P pulmonale (P wave amplitude of 2.5 mm (0.25 mV) in
leads II, III, and a VF), or an S1Q3 (S1Q3T3) pattern.67,68
ECG tracings are also of value in establishing the
diagnosis of dysrhythmias associated with COPDin
particular, multifocal atrial tachycardia (MAT). This
arrhythmia is commonly mistaken for atrial fibrillation, and
incorrect intervention may be undertaken as a result. The
term MAT was coined in 1968 by Shine et al, who
described it as having the following characteristics:69
Atrial rate of greater than 100/min
Three or more morphologically distinct P waves
Irregular P-P intervals
Isoelectric baseline between P waves
In addition to oxygen, inhaled -agonists and anticholinergics are the cornerstones of therapy for acute exacerbations of COPD. Medications can be given by either smallvolume nebulizer or MDI with spacer. The mode of delivery
is not important for most patients with acute exacerbations
of COPD. Berry et al conducted a prospective, crossover
double-blind trial of these modes in 20 patients admitted to
the hospital for acute exacerbations of COPD.73 They found
no significant differences in the FEV1, forced vital capacity
(FVC), or Borg dyspnea score when comparing MDI to
nebulization. A recent systematic review of the literature
also found no difference in clinical effectiveness between
nebulizers and MDIs in patients with COPD.74
The addition of a spacer chamber is an important adjunct
when using the MDI and dramatically increases effective drug
delivery.75 Most of the literature documenting the equivalence of MDIs and nebulizers involves the use of a spacer
and has been limited to patients with mild-to-moderate
exacerbations. Patients do not need to be able to hold their
breath for 10 seconds when using MDIs with spacers. One
recent study showed that taking six normal tidal breaths per
puff (using a spacer chamber) is therapeutically equivalent
Hypoxemia is the most common underlying

cause of MAT. Therapy involves reversing the hypoxia
not anti-arrhythmics. Other causes for MAT include
CHF and electrolyte imbalances (hypokalemia and
hypomagnesemia).70
April 2002
to the traditional (and more difficult) two maximal breaths

with a breath-hold.76
From a practical perspective, the treatment of acute
asthma and acute exacerbations of COPD differs in some
important ways. First, the COPD may or may not be
reversible, so that an anticipated improvement in PEFR or
FEV1 may not occur despite subjective clinical improvement. Second, the use of 2-agonists may not be as helpful in
COPD, since wheezing may be more a function of fixed
airway obstruction than bronchospasm.
Anticholinergics are very useful in COPD, as muscarinic receptors (M1, M2, and M3) play a significant role in
respiratory pathology. Ipratropium is an example of a nonspecific muscarinic antagonist with few systemic side
effects. Karpel et al studied the effects of ipratropium and
metaproterenol on patients presenting with acute exacerbations of COPD and found that both improved FEV1 and
FVC, but that the 2-agonist caused a significant drop in
PaO2 as well as an increase in adrenergic side effects.77
McCrory and Brown systematically reviewed studies of
inhaled 2-agonists vs. ipratropium in patients with acute
exacerbations of COPD and found few relevant studies that
compared the two in the acute setting. While they both
improved FEV1, the results were not statistically significant,
and neither was superior.66 While the lack of statistical
significance may be due to relatively small numbers of
patients (there were little more than 100 patients in these
studies), a more likely explanation involves the absence of
reversible pathology in COPD.
patients with asthma, there are only observational data

regarding their efficacy in COPD. One group conducted a
population-based cohort study of an administrative
database in Canada.86 They found that patients who were
prescribed inhaled corticosteroids within 90 days of
discharge had 24% fewer hospitalizations (95% CI, 22%35%) and 29% less mortality than the cohort not receiving
inhaled corticosteroids (95% CI, 22%-35%).
Corticosteroids
While there is a small percentage of COPD patients for
whom corticosteroids improve outcome, it is not always
possible to predict who these patients are. Wood-Baker et al
systematically reviewed the use of oral corticosteroids in
acute exacerbations of COPD.87 They noted a significant
improvement in FEV1, but this was not sustained past 72
hours. In their review, there were fewer treatment failures
with IV or PO steroids.
Dosing and route of steroid administration vary widely.
ED dosages may vary from 0.5-1.5 mg/kg for oral or
parenteral steroids, and the subsequent doses may range
from 0.5-1.0 mg/kg per day for several days to a week.
Short-term steroids are associated with a small increase in
increase in adverse events, such as hyperglycemia.
While the literature remains spotty, oral corticosteroids
may suffice for most ED patients with an acute exacerbation
of COPD.
Methylxanthines
Barr et al systematically reviewed methylxanthines
(i.e., aminophylline) in acute exacerbations of COPD and
found that the use of aminophylline did not significantly improve
FEV1 and had no effect on hospital admission.88 If a patient
comes to the ED with an acute exacerbation of COPD and is
already on theophylline, check a serum theophylline level.
Adverse events secondary to toxicity, including death, are
more common among those with chronic use of theophylline. In a prospective study by Shannon, elderly patients
were more likely to experience severe toxicity, including
fatal cardiac arrhythmias.89
Combination Therapy
Multiple studies show that the combination of albuterol and
ipratropium provides superior bronchodilation than treatment
with either component alonewithout additional side effects.78-81
The combination of -agonists and anticholinergics may be
cost-effective as well. In one controlled trial, over 1000
patients were randomized to ipratropium alone, albuterol
alone, or the combination therapy. When the total costs of
therapy were examined (including costs associated with
decompensation and hospitalization), combination therapy
was less expensive than albuterol alone.82
Antibiotics
Dosing
Some patients with acute exacerbations of COPD benefit

from antibiotic therapy. Indications for antibiotics are based
on the Anthonisen criteria: increased dyspnea, increased
sputum volume, and sputum purulence. Anthonisen et al used
these criteria in their classic study of 362 patients with acute
exacerbations of COPD. Patients were treated with two
weeks of trimethoprim-sulfamethoxazole, amoxicillin, or
doxycycline vs. placebo using a crossover design. Patients
with the aforementioned criteria who received antibiotics
showed more rapid improvement in PEFR and had fewer
treatment failures.63 The GOLD guidelines also support the
use of antibiotics in acute exacerbations of COPD when the
Anthonisen criteria are met.4 In at least one study, patients
with severe functional impairment and a higher number of
exacerbations per year derived the greatest benefit from
antibiotic treatment.90
The dosing of albuterol in acute exacerbations of COPD is

generally 2.5-5.0 mg via nebulizer every 20 minutes as
needed or with continuous nebulization 10-15 mg/hr. Data
on continuous nebulization in patients with COPD are
scarce. While MDI treatments are usually given as four
puffs, some data indicate that 11 puffs are therapeutically
equal to 2.5 mg of nebulized albuterol.83 Studies in asthma
employ 6-12 puffs per treatment using an albuterol MDI,
even in children.84 Ipratropium can be added to the albuterol
in a dose of 0.5 mg per nebulization or by four puffs using
an MDI with spacer.85
When using a nebulizer in patients who are prone to
CO2 retention, have the respiratory therapist hook it up to
compressed air rather than oxygen.
Inhaled Corticosteroids
While inhaled corticosteroids appear to be beneficial in
April 2002
Continued on page 13
Clinical Pathway: Emergency Department Therapy

For Acute Exacerbations Of COPD
Upright sitting position (Class indeterminate)

Oxygen therapy (Class I)
Pulse oximetry (Class I-II)
Cardiac monitor (Class indeterminate)
IV access (Class II-III)
Respiratory arrest?
Severe dyspnea or profound tachypnea?
Yes
Life-threatening hypoxemia?
Severe acidosis or severe hypercapnia?

Somnolence?
Shock?
Intubate using RSI technique (Class I-II)

Ventilate with prolonged expiratory phase
Low tidal volumes
Low rate
No
Short-acting -agonist (Class I-II)

Albuterol 2.5-5 mg via nebulizer or 4-10 puffs via MDI
plus spacer (repeat as needed q20-60min)
Plus ipratropium (Class I-II)
0.5 mg q20min via nebulizer or 4-6 puffs via MDI plus
spacer (repeat as needed q20-60min)
Plus steroids (Class III)
Prednisone 40-60 mg PO or methylprednisolone 125 mg IV
O2 saturation 90% despite high-flow O2?

Yes
Moderate acidosis (pH 7.30-7.35)?
Moderate-to-severe dyspnea?
Respiratory rate > 25 breaths per minute?
Consider NIV if no contraindications (Class II)
Go to top of next page
The evidence for recommendations is graded using the following scale. For complete definitions, see back page. Class I: Definitely recommended.
Definitive, excellent evidence provides support. Class II: Acceptable and useful. Good evidence provides support. Class III: May be acceptable,
possibly useful. Fair-to-good evidence provides support. Indeterminate: Continuing area of research.
This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a
patients individual needs. Failure to comply with this pathway does not represent a breach of the standard of care.
Copyright 2002 EB Practice, LLC. EB Practice, LLC (1-800-249-5770) grants each subscriber limited copying
privileges for educational distribution within your facility or program. Commercial distribution to promote any
product or service is strictly prohibited.
10
April 2002

(continued)
Fever?
Significant distress?
Heart disease?
Intravenous drug abuse?
Seizures?
Immunosuppression?
Other pulmonary disease?
Prior thoracic surgery?
Diagnosis unclear?
Chest x-ray* (Class I-II)

Yes
*Some authorities suggest routine chest x-rays in acute

exacerbations of COPD
No
Altered mental status?

Severe distress?
Suspected acidosis?
Persistent hyperventilation?
Intractable hypoxia?
Central cyanosis?
Signs of right heart failure?
Yes
Arterial blood gas (Class II-III)
No
Ischemic-sounding chest pain?

Suspicious jaw, shoulder, neck, arm, back,
Yes
or abdominal pain?
Severe distress?
Irregular heart rate?
Signs of right heart failure?
ECG (Class I-II)
No
Directed laboratory testing:

Theophylline level if patient on theophylline product (Class II)
Cardiac enzymes if suspicion for acute coronary syndrome (Class I-II)
B-natruretic peptide if possible but unclear diagnosis of CHF (Class II-III)
Electrolytes if vomiting, weakness, diuretics, or renal failure (Class II)
Third-generation d-dimer plus dead space analysis if suspicion of PE or DVT (Class II-III)
Go to top of next page
April 2002
11

(continued)
Directed imaging studies:

Helical CT angiography of the chest or V/Q scan if suspicion of PE (Class II)
Echocardiography if suspicion of acute, first-time episode of CHF (Class II-III)
Severe dyspnea?
Confusion or lethargy?
Worsening acidemia, hypoxemia, and
hypercapnia?
Mechanical ventilation?
Yes
Admit to ICU (Class I-II)
No
Failure to respond to ED management?

Newly occurring dysrhythmias?
Significant comorbidities?
Diagnostic uncertainty?
Yes
Admit to floor (Class II)
No
Recent history of increased dyspnea?

Increased sputum volume?
Sputum purulence?
Yes
Prescribe oral antibiotics for 10-14 days (Class II)
Yes
Discharge home (Class II)

Encourage smoking cessation
Ensure patient has all needed prescriptions and knows
follow-up instructions
No
Patient responded well to ED therapy?

Able to take PO?
No
Admit to observation unit if available; otherwise, admit

to floor (Class II)
12
April 2002
Continued from page 9
able to cooperate with instructions. Ensure that they can

manage their secretions and that appropriate staffing levels
and monitoring facilities are available.
Contraindications to NIV include apnea, pneumothorax, inability to protect the airway, and altered mental status
(including severe agitation). Other exclusion criteria include
cardiovascular instability (hypotension, arrhythmias,
myocardial infarction), high aspiration risk, viscous or
copious secretions, recent facial or gastroesophageal surgery,
craniofacial trauma, fixed nasopharyngeal abnormalities,
and extreme obesity.4
Assisted Ventilation
When COPD is complicated by respiratory failure, hypoxia
and respiratory acidosis ensue. Unless timely ventilatory
assistance is given, worsening respiratory failure and death
are likely to follow. The traditional intervention has been
endotracheal intubation and mechanical ventilation. In
recent years, there has been an increased interest in the use
of NIV in COPD. Some have even proposed it as a new
standard of care.91 While NIV in emergency medicine has
been comprehensively reviewed in a recent edition of this
publication (see the July 2001 issue of Emergency Medicine
Practice, Noninvasive Airway Management Techniques:
How And When To Use Them), several points should
be reinforced.
CPAP vs. BiPAP

NIV can be provided via many standard ventilators or,
alternatively, by a separate bedside apparatus. Either
volume-limited or pressure-limited systems can be used.
Both bi-level positive airway pressure (BiPAP) and continuous positive airway pressure (CPAP) modes are pressurecontrolled devices. BiPAP delivers continuous positive
airway pressure but allows for different levels of inspiratory
and expiratory support. CPAP delivers a static airway
pressure throughout the respiratory cycle. Machines are
initially set at low pressures, and the pressures are
increased as needed. For CPAP, starting pressures are
typically 5 cmH2O. For BiPAP, inspiratory settings
typically begin at 8-10 cmH2O with expiratory pressures
in the 2-4 cmH2O range.
Utility
NIV augments respiratory function and improves alveolar
ventilation by increasing tidal volume and preventing
collapse of distal airways. This reduces the respiratory work
and can improve both clinical parameters and gas exchange.
Multiple well-designed studies show that in properly
selected patients with COPD, NIV improves blood gases
and pH, reduces the need for tracheal intubation, and
decreases length of hospital stay.4,92-95 Brochard et al demonstrated a reduction in mortality, complications, and length of
stay when NIV was compared with traditional means of
invasive ventilation in patients with COPD.91 Plant et al
showed that NIV was both feasible and beneficial outside
the setting of the ICU.96 The Joint Guidelines support the
role of NIV in COPD.97 While NIV is clearly beneficial in
select patients with COPD, the literature shows mixed
results in patients with asthma.
Advantages/Disadvantages
In the proper circumstances, NIV offers several advantages
over intubation. Patients can be managed outside of the ICU
setting, which reduces ICU time and expense. Complications such as pneumonia occur less commonly, and overall
mortality is reduced. (Plus, who wants to be intubated?)
However, NIV is not without its problems. Some
patients find the mask very uncomfortable and experience
claustrophobia. If facemasks or nasal masks are ill-fitting,
significant air leaks can develop, rendering NIV ineffective.
If the masks are too tight, skin excoriation can develop.
Gastric distension and barotraumas may occur.
Even when patients have been carefully selected, NIV
can fail. Close observation and careful patient monitoring
will allow early detection of impending failure and facilitate
timely endotracheal intubation.
Patient Selection
To obtain maximum benefits, the decision to use NIV in
COPD exacerbation must be made early.96 If supplemental
oxygen provided by non-rebreather mask cannot maintain
oxygen saturation above 90%, consider the need for assisted
ventilation. Other indications include moderate acidosis
(pH 7.30-7.35), moderate-to-severe dyspnea, and respiratory
rate greater than 25 breaths per minute.
Patients must be alert, breathing spontaneously, and
Cost-Effective Strategies For Patients With COPD

1. Encourage the patient to stop smoking.
One cost-effectiveness analysis suggested that smoking
cessation across the entire population would increase life
expectancy by several years. The cost of intervention would
be $705-998 per year of life saved for males and $1204-$2058
per year of life saved for females.117 (However, one study
commissioned by Philip Morris in the Czech Republic found
that cigarette smoking saved the government $24-$30
million dollars in healthcare, pensions, and public housing
due to the shortened life of the average smoker.)
an anticholinergic.
In one study, the combination of albuterol and ipratropium
was ultimately less expensive in terms of total health costs
than using ipratropium alone.82
3. Institute early NIV in suitable candidates.
One meta-analysis of NIV vs. standard therapy showed
a cost savings per patient admission of $3244 Canadian
for every patient treated with NIV compared to
mechanical ventilation.118
Caveat: Ensure that patients treated with NIV have no
contraindications to its use. (See text.)
2. Treat patients with both a short-acting 2-agonist and
April 2002
13
Intubation
Most authorities recommend a short inspiratory time,

prolonged expiratory time, and decreased minute ventilation.104 Jain et al suggest initial ventilatory settings of assist
control, 100% oxygen, a respiratory rate of 8-10, peak
inspiratory flow of 80-100 L/min, and a PEEP of 0. Physiologic goals at this setting include a plateau airway pressure
of 30 cmH2O or less and a volume at end inspiration of 20
cc/kg or less or 1.4 L. If the patient does not improve, they
suggest changing the ventilator settings to synchronized
intermittent mandatory ventilation or pressure support
mode (preferably with a low tidal volume of 6-8 cc/kg and
a respiratory rate of 8-10/min).105 The addition of an end
inspiratory pause in patients with COPD may be detrimental.106 Side effects such as high peak pressures and hypercapnia are generally well-tolerated.
The strategy of permissive hypercapnia (mild hypoxia
and high PCO2) is not as well-studied in COPD as in the
adult respiratory distress syndrome (ARDS).
Do not try to obtain eucapnia (a normal PCO2)
in intubated patients who are chronic retainers.
Rapidly blowing off their CO2 will result in a sudden
metabolic alkalosis secondary to their chronically
elevated bicarbonate.
The need to intubate can be starkly obvious in some cases

and an agonizing choice in others. The GOLD guidelines
suggest indications for invasive mechanical ventilation.
They include:4
Severe dyspnea with use of accessory muscles
Respiratory rate greater than 35 breaths per minute
Life-threatening hypoxemia (PaO2 < 40 mmHg or
PaO2/FiO2 < 200 mmHg)
Severe acidosis (pH < 7.25) and hypercapnia (PaCO2
> 60 mmHg)
Respiratory arrest
Somnolence or impaired mental status
Cardiovascular complications (hypotension, shock,
heart failure)
Other complications (metabolic abnormalities, sepsis,
pneumonia, PE, barotrauma, massive pleural effusion)
Nasal intermittent positive pressure ventilation
(NIPPV) failure
Many of these indications allow for quite a bit of
judgment (e.g., respiratory rate, pneumonia), while others
are quite firm (respiratory arrest).
While the choice of orotracheal vs. nasotracheal
intubation may be left to the discretion of the emergency
physician, most ED intubations currently employ
oral-tracheal intubation using a rapid sequence
intubation technique.
The decision to paralyze a patient prior to intubation
requires the physician to estimate the degree of difficulty
involved in passing a tube through the cords in a
particular patient. (See the May 2000 issue of Emergency
Medicine Practice, Emergency Endotracheal Intubations:
An Update On The Latest Techniques.) Patients with
an anticipated nightmare airway may be better served
with an awake intubation.
The choice of inductions agents varies among institutions, but etomidate has a particularly appealing safety
profile.98,99 While the use of ketamine as an induction agent
has been studied in asthmatics (with varying success), there
is no good literature regarding its use in COPD. Succinylcholine 1.5 mg/kg remains the muscle relaxant of choice in
many EDs, although the non-depolarizing blocker
rocuronium is finding favor in some.100
When intubating a patient with COPD, use the largest
endotracheal tube that fits through the cords, as this will
reduce the airway resistance. This generally translates to an
8.0-8.5 F for males, and a 7.5-8.0 F for females.
The use of positive end-expiratory pressure (PEEP) in
intubated patients with COPD is controversial. Tuxen found
that PEEP resulted in potentially dangerous increases in
lung volume and circulatory compromise.101 Pepe and
Marini noted that patients with COPD were more susceptible to PEEP, as their lungs more readily transmitted
alveolar pressure to intrathoracic vessels.102 Sydow et al,
however, noted that PEEP may be used in patients recovering from acute exacerbations of COPD, as it may decrease
the inspiratory work of breathing.103
The optimum ventilator settings remain unknown.
Management Of Ventilator Associated Hypotension

Hemodynamic compromise after intubation should
prompt a rapid search for pneumothorax vs. dynamic
hyperinflation (too much air pumped into the lungs).101,102,107
Dynamic hyperinflation can be misinterpreted as pneumothorax, with potentially disastrous results. Before
inserting a 14-gauge catheter into the second intercostal
space, it is wise to disconnect the patient from the ventilator
for one minute. If dynamic hyperinflation is the problem,
the blood pressure should normalize as the hyperinflation is
relieved and blood can once again return to the right heart.
Restraint in sticking a needle into the chest is especially
important when the patient has no other signs of tension
pneumothorax (e.g., distended neck veins, tracheal deviation, decreased breath sounds, asymmetric chest rise).
Special Circumstances
Two interventions should be considered for patients
with acute exacerbations of COPD who present to the
ED: smoking cessation and flu vaccination. While these
issues cannot be comprehensively accomplished in the
ED visit, discussing them with the patient may facilitate
follow-up care.
Smoking cessation is the only proven method to decrease the
decline in lung function and is ultimately the most important
treatment of COPD. The benefits of smoking cessation are
greatest when the smoker quits early in life.4,108,109 A systematic review of influenza vaccination in patients with COPD
demonstrated a reduction in exacerbations.110
Controversies/Cutting Edge
Lung Volume Reduction Surgery
Lung volume reduction surgery is a promising intervention
14
April 2002
COPD as an antioxidant. A recent meta-analysis of published double-blind, placebo-controlled clinical trials

concluded that with prolonged use, oral NAC prevents
exacerbations and may decrease morbidity and healthcare
costs.113 There is no evidence to suggest that NAC has any
role to play in acute exacerbations of COPD.
that can be recommended only for carefully selected

patients.111 Patients should discuss this and other
options (e.g., home O2) with the pulmonologist and
thoracic surgeon.
Role Of Heliox
Heliox is a mixture of helium and oxygen and has a lower
density than nitrogen-oxygen mixtures. It can decrease
turbulent airflow in obstructed airways and in theory
reduce the work of breathing. Although heliox has been
investigated in COPD, few randomized, controlled trials
have been reported. One such study by deBoisblanc et al
compared heliox to compressed air as the vehicle to deliver
bronchodilators in patients with COPD. Heliox failed to
show any clinical benefit compared to air alone.112
Disposition
The GOLD guidelines suggest admission for any patient
with an acute exacerbation of COPD who fails to respond
to initial medical management, has newly occurring
dysrhythmias or significant comorbidities, or in whom
there is diagnostic uncertainty. ICU admission is suggested
for patients who present with severe dyspnea, confusion
or lethargy, and worsening acidemia, hypoxemia,
and hypercapnia.
Once the patient is stable, it is important to determine
why this exacerbation occurred. Consider an underlying
infection, co-morbid illness (such as CHF or PE), and
medication noncompliance.
N-acetylcysteine
In the past, inhaled N-acetylcysteine (NAC) was used as a
mucolytic (Mucomyst). There is little literature to support its
use for this purpose.
However, oral NAC has been used in chronic stable
Ten Excuses That Dont Work In Court

While designated areas make the treatment of some diseases
more efficient, they may create a false sense of diagnostic
certainty. Determine whether the patient feels that the current
attack is business as usual or something different.
1.I didnt hear any wheezing, so I assumed the patient

was okay.
The absence of wheezing does not exclude the diagnosis of
obstructive pulmonary disease. Further, a silent chest in a
dyspneic patient is an ominous sign.
7. I thought the vomiting was from gastroenteritis and the

tremor was from from his albuterol. I didnt order an
aminophylline level because he was taking his usual dose.
This patient developed near-fatal arrhythmias and had an
aminophylline level of 48. Aminophylline toxicity is a
dangerous condition that cannot be diagnosed by history
alone. Get a level!
2.He got better on the non-rebreather mask; it was a lot

better than the two liters of nasal cannula he was getting at
home. He then got very sleepy, so we closed the door, turned
out the lights, and let him rest.
Thank your stars that an alert environmental services person
let the charge nurse know that the guy in room 4 doesnt look
so good. Patients with COPD who are placed on high-flow
oxygen must be closely monitored for CO2 narcosis.
8.The nurse didnt tell me that she was getting worse.

Many EDs have standing orders that allow the nurse to
give the first dose of inhaled therapy upon the patients
arrival. However, it is wise for the physician to examine
the patient as soon as possible. This allows for consideration
of dangerous mimics, co-morbid disease, and recognition of
early deterioration.
3.She told me she had asthma, so I kept giving her

albuterol. Later she went into respiratory failure, and I
couldnt intubate her.
Women with COPD are more likely than men to remain
undiagnosed. While the treatment of asthma and COPD often
overlap, this lady could have benefited from ipratropium and
perhaps early NIV.
9.We never suspected that the patient had a PE.

Patients who die of pulmonary embolism tend to be older
and sicker (just like patients with COPD). Assess for
thromboembolic risk factors in patients with sudden-onset
dyspnea and use objective tests such as third-generation
d-dimers, dead-space analysis, and CT angiography when
clinical suspicion is high.
4.He seemed to be doing well on CPAP, so I admitted him to

the floor.
Patients on NIV must be admitted to an area in which they can
be monitored closely.
5.I didnt give the patient albuterol because she has COPD,
and that is not a reversible airway disease.
While most acute exacerbations of COPD will respond
minimally to inhaled 2-agonists, it is important to offer this
therapy for the 10% with wheezy bronchitis. Such patients
may improve dramatically.
10.We stopped doing admission chest radiographs as a costcutting measure.

This patient died of pneumonia-associated sepsis. While a
decrease in test ordering is commendable, skipping chest
films in an ill-appearing patient with COPD is risky. Important
alternative diagnoses may be made, such as pneumonia, PE, or
fluid overload from either CHF or renal failure.
6.He was sitting in the asthma room. We never suspected his

chest pain could be an MI.
April 2002
15
Discharge Medications
4.*
Along with continuing short-acting 2-agonists and

anticholinergics, consider prescribing oral corticosteroids.
Long-acting 2-agonists and long-acting anticholinergics
may be added with strict patient education on which
medicines are rescue-types (to be used with acute
symptoms) and which are controller-types (to be used as
chronic therapy).
Appleton et al systematically reviewed the literature on
the efficacy of long-acting 2-agonists, specifically salmeterol
and formoterol, on various outcomes on COPD. They found
that 50 mcg of salmeterol twice a day had no effect on
relapse rate, increased FEV1 only slightly, but reduced
breathlessness and significantly improved the quality of
life.114 Another large study showed that salmeterol produced
a more constant bronchodilatory effect than a short-acting
agent with no evidence of bronchodilator tolerance.115
There is growing evidence regarding the efficacy of
once-daily dosing of the long-acting anticholinergic
tiotropium. The Dutch Tiotropium Study Group found that
18 mcg tiotropium was more efficacious than four times
daily dosing of 40 mcg ipratropium in improving pulmonary function in COPD patients.116 There was no increase in
side effects.
5.*
6.*
7.*
8.
9.
10.
11.
12.*
13.*
Summary
14.
The diagnosis and treatment of COPD continue to evolve.

Since patients may not be diagnosed as COPD prior to the
ED visit, emergency physicians must suspect COPD in
patients who present with cough, dyspnea, and sputum
production. While similar to asthma in some ways, there are
important differences in the pathophysiology and treatment,
most notably in the area of NIV. With appropriate treatment
and disposition, relapse, morbidity, and mortality may be
significantly reduced and quality of life improved.
15.
16.*
17.*
18.*
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Evidence-based medicine requires a critical appraisal of the

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included in bold type following the reference, where
available. In addition, the most informative references cited
in the paper, as determined by the authors, will be noted by
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106. Georgopoulos D, Mitrouska I, Markopoulou K, et al. Effects of
breathing patterns on mechanically ventilated patients with chronic
obstructive pulmonary disease and dynamic hyperinflation. Intensive
Care Med 1995 Nov;21(11):880-886. (Randomized, controlled trial; 9
patients)
107.* Williams TJ, Tuxen DV, Scheinkestel CD, et al. Risk factors for
morbidity in mechanically ventilated patients with acute severe
asthma. Am Rev Respir Dis 1992 Sep;146(3):607-615. (Retrospective, 88
patients; prospective, 22 patients)
108.* Pride NB. Smoking cessation: effects on symptoms, spirometry and
future trends in COPD. Thorax 2001 Sep;56 Suppl 2:ii7-10. (Review)
109.* Xu X, Dockery DW, Ware JH, et al. Effects of cigarette smoking on rate
of loss of pulmonary function in adults: a longitudinal assessment. Am
Rev Respir Dis 1992 Nov;146(5 Pt 1):1345-1348. (Cross-sectional; 8191
patients)
110.* Cates CJ, Jefferson TO, Bara AI, et al. Vaccines for preventing influenza
in people with asthma (Cochrane Review). Cochrane Database Syst Rev
2000;(4):CD000364. (Systematic review)
111. Hensley M, Coughlan JL, Gibson P. Lung volume reduction surgery
for diffuse emphysema(Cochrane Review). Cochrane Database Syst Rev
2000;2. (Systematic review)
112. deBoisblanc BP, DeBleiux P, Resweber S, et al. Randomized trial of the
use of heliox as a driving gas for updraft nebulization of
bronchodilators in the emergent treatment of acute exacerbations of
chronic obstructive pulmonary disease. Crit Care Med 2000
Sep;28(9):3177-3180. (Randomized, controlled trial; 25 patients)
113. Grandjean EM, Berthet P, Ruffmann R, et al. Efficacy of oral long-term
N-acetylcysteine in chronic bronchopulmonary disease: a metaanalysis of published double-blind, placebo-controlled clinical trials.
Clin Ther 2000 Feb;22(2):209-221. (Meta-analysis)
114.* Appleton S, Smith B, Veale A, et al. Long-acting beta2-agonists for
chronic obstructive pulmonary disease. Cochrane Database Syst Rev
2000;(2):CD001104. (Systematic review)
115.* Rennard SI, Anderson W, ZuWallack R, et al. Use of a long-acting
inhaled beta2-adrenergic agonist, salmeterol xinafoate, in patients with
chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001
Apr;163(5):1087-1092. (Randomized, controlled trial; 405 patients)
116.* van Noord JA, Bantje TA, Eland ME, et al. A randomised controlled
comparison of tiotropium and ipratropium in the treatment of chronic
obstructive pulmonary disease. The Dutch Tiotropium Study Group.
Thorax 2000;55:289-294. (Randomized, controlled trial)
controlled trial; 20 patients)

Brocklebank D, Ram F, Wright J, et al. Comparison of the effectiveness
of inhaler devices in asthma and chronic obstructive airways disease: a
systematic review of the literature. Health Technology Assessment
(Winchester, England) 2001;5(26):1-149. (Review; 354 references)
Hindle M, Chrystyn H. Relative bioavailability of salbutamol to the
lung following inhalation using metered dose inhalation methods and
spacer devices. Thorax 1994 Jun;49(6):549-553. (Controlled; 10 patients)
Eiser NM, Phillips C, Wooler PA. Does the mode of inhalation affect
the bronchodilator response in patients with severe COPD? Respir Med
2001 Jun;95(6):476-483. (Randomized, controlled trial; 20 patients)
Karpel JP, Pesin J, Greenberg D, et al. A comparison of the effects of
ipratropium bromide and metaproterenol sulfate in acute exacerbations of COPD. Chest 1990 Oct;98(4):835-839. (Controlled; 32 patients)
Friedman M. Combined bronchodilator therapy in the management of
chronic obstructive pulmonary disease. Respirology 1997;2 Suppl 1:S19S23. (Review; 24 references)
Campbell S. For COPD a combination of ipratropium bromide and
albuterol sulfate is more effective than albuterol base. Arch Intern Med
1999 Jan 25;159(2):156-160. (Randomized, controlled trial; 357
patients)
Gross N, Tashkin D, Miller R, et al. Inhalation by nebulization of
albuterol-ipratropium combination (Dey combination) is superior to
either agent alone in the treatment of chronic obstructive pulmonary
disease. Dey Combination Solution Study Group. Respiration
1998;65(5):354-362. (Randomized, controlled trial; 863 patients)
No authors listed. Routine nebulized ipratropium and albuterol
together are better than either alone in COPD. The COMBIVENT
Inhalation Solution Study Group. Chest 1997 Dec;112(6):1514-1521.
(Randomized, controlled trial; 652 patients)
Friedman M, Serby CW, Menjoge SS, et al. Pharmacoeconomic
evaluation of a combination of ipratropium plus albuterol compared
with ipratropium alone and albuterol alone in COPD. Chest 1999
Mar;115(3):635-641. (Randomized, controlled trial; 1067 patients)
Rodrigo C, Rodrigo G. Salbutamol treatment of acute severe asthma in
the ED: MDI versus hand-held nebulizer. Am J Emerg Med 1998
Nov;16(7):637-642. (Randomized, controlled trial)
Robertson CF, Norden MA, Fitzgerald DA, et al. Treatment of acute
asthma: salbutamol via jet nebuliser vs spacer and metered dose
inhaler. J Paediatr Child Health 1998 Apr;34(2):142-146. (Randomized,
controlled trial; 160 children)
Friedman M. A multicenter study of nebulized bronchodilator
solutions in chronic obstructive pulmonary disease. Am J Med 1996 Jan
29;100(1A):30S-39S. (Randomized, controlled trial; 213 patients)
Sin DD, Tu JV. Inhaled corticosteroids and the risk of mortality and
readmission in elderly patients with chronic obstructive pulmonary
disease. Am J Respir Crit Care Med 2001 Aug 15;164(4):580-584.
(Population-based cohort study; 22,620 patients)
Wood-Baker R, Walters EH, Gibson P. Oral corticosteroids for acute
exacerbations of chronic obstructive pulmonary disease. Cochrane
Database Syst Rev 2001;(2):CD001288. (Systematic review)
Barr RG, Rowe BH, Camargo CA Jr. Methyl-xanthines for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst
Rev 2001;(1):CD002168. (Systematic review)
Shannon M. Life-threatening events after theophylline overdose: a 10year prospective analysis. Arch Intern Med 1999 May 10;159(9):989-994.
Allegra L, Blasi F, de Bernardi B, et al. Antibiotic treatment and
baseline severity of disease in acute exacerbations of chronic
bronchitis: a re-evaluation of previously published data of a placebocontrolled randomized study. Pulm Pharmacol Ther 2001;14(2):149-155.
Brochard L. Non-invasive ventilation for acute exacerbations of COPD:
a new standard of care. Thorax 2000 Oct;55(10):817-818. (Editorial)
Celikel T, Sungur M, Ceyhan B, et al. Comparison of noninvasive
positive pressure ventilation with standard medical therapy in
hypercapnic acute respiratory failure. Chest 1998 Dec;114(6):1636-1642.
Kramer N, Meyer TJ, Meharg J, et al. Randomized, prospective trial of
noninvasive positive pressure ventilation in acute respiratory failure.
Am J Respir Crit Care Med 1995 Jun;151(6):1799-1806. (Randomized,
controlled trial)
Bott J, Carroll MP, Conway JH, et al. Randomised controlled trial of
nasal ventilation in acute ventilatory failure due to chronic obstructive
airways disease. Lancet 1993 Jun 19;341(8860):1555-1557. (Randomized,
controlled trial; 60 patients)
Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med
2001 Feb;163(2):540-577. (Review)
18
April 2002
117.* Tsevat J. Impact and cost-effectiveness of smoking interventions. Am J

Med 1992; 93(1A):43S-47S. (Review; 35 references)
118. Keenan SP, Gregor J, Sibbald WJ, et al. Noninvasive positive pressure
ventilation in the setting of severe, acute exacerbations of chronic
obstructive pulmonary disease: More effective and less expensive. Crit
Care Med 2000;28:2094-2102. (Meta-analysis and economic evaluation
of treatment)
56. In mild-to-moderate exacerbations of COPD, which

of the following statements regarding the route of 2agonists is true?
a. Subcutaneous delivery is preferred to inhaled
delivery.
b. MDI and nebulization are equally effective.
c. The nebulized route is superior to MDI.
d. Oral and inhaled routes are equally effective.
Physician CME Questions
57. Which of the following clinical parameters is the

most reliable indicator of ventilatory failure?
a. Worsening wheeze and cough
b. Inability to answer in sentences without interruption for additional breaths
c. Failure to improve pulse oximeter above 90% on
room air
d. Mental status deterioration in spite of adequate
treatment
49. Which of the following has been shown to slow the

progression of COPD?
a. Long-term oral steroid use
b. Prophylactic antibiotics during the winter months
c. Administration of annual flu vaccines
d. Cessation of smoking
50. Which of the following is not considered a risk factor
for COPD?
a. 1-antitrypsin deficiency
b. Industrial pollution
c. Tobacco smoking
d. Asian ethnicity
58. All of the following statements are true of

noninvasive ventilation in COPD except:
a. NIV is better tolerated than endotracheal intubation.
b. NIV can be used intermittently.
c. NIV has been shown to be a cost-effective management strategy.
d. NIV should be considered when the pH is less
than 7.35.
51. Which of the following features is most helpful in

differentiating COPD from asthma in the ED?
a. History of smoking
b. Age of the patient
c. Presence of wheeze
d. Reversibility of bronchospasm with
bronchodilators
59. A patient with known COPD required intubation for

respiratory failure. Following successful intubation,
the patient was placed on a ventilator. Immediately
following this, the patient developed hemodynamic
compromise. Which of the following is your immediate diagnostic concern?
a. Pulmonary embolus
b. Tension pneumothorax
c. Atelectasis
d. Pneumonia
52. The GOLD classification defines stage II (moderate)

COPD as which of the following?
a. FEV1 80% but 60% predicted
b. FEV1 80% but 50% predicted
c. FEV1 80% but 40% predicted
d. FEV1 80% but 30% predicted
53. Which of the following cells predominate and
mediate damage in COPD?
a. CD4 lymphocytes
b. CD8 lymphocytes
c. Macrophages
d. Neutrophils
60. All of the following are true of multifocal atrial

tachycardia (MAT) except:
a. MAT is a common tachydysrhythmia in COPD.
b. MAT can occur from theophylline toxicity.
c. MAT cannot be distinguished from atrial fibrillation on palpation alone.
d. Digoxin is the treatment of choice.
54. All of the following are indicated in the patient with a

moderate exacerbation of COPD except:
a. supplemental oxygen.
b. intravenous access.
c. methylxanthines.
d. inhaled 2-agonists.
61. The most dangerous complication of theophylline

toxicity is:
a. syncope.
b. cardiac dysrhythmias.
c. seizure.
d. chest pain.
55. Which of the following statements about PE in

patients with pre-existing COPD is true?
a. ABG is a helpful diagnostic test.
b. V/Q scan alone is usually adequate to make the
diagnosis.
c. Thrombolysis is favored over heparin for treatment.
d. False-negative spiral CT angiograms and falsepositive V/Q scans are more common than in
patients without COPD.
April 2002
62. Multiple studies show that the combination

of albuterol and ipratropium provides
superior bronchodilation than treatment with
either component alonewithout additional
side effects.
a. True
b. False
19
Physician CME Information
63. All of the following are true of inhaled anticholinergic agents in COPD except:
a. Their actions are mediated through muscarinic
receptors.
b. They work in a synergic manner with -agonists.
c. They are associated with very few side effects.
d. Used alone, they are superior to -agonists in
COPD.
This CME enduring material is sponsored by Mount Sinai School of Medicine

and has been planned and implemented in accordance with the Essentials
and Standards of the Accreditation Council for Continuing Medical
Education. Credit may be obtained by reading each issue and completing
the post-tests administered in December and June.
Target Audience: This enduring material is designed for emergency
medicine physicians.
Needs Assessment: The need for this educational activity was
determined by a survey of medical staff, including the editorial board
of this publication; review of morbidity and mortality data from the
CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for
emergency physicians.
Date of Original Release: This issue of Emergency Medicine Practice was
published April 1, 2002. This activity is eligible for CME credit through April
1, 2005. The latest review of this material was March 15, 2002.
Discussion of Investigational Information: As part of the newsletter, faculty
may be presenting investigational information about pharmaceutical
products that is outside Food and Drug Administration approved labeling.
Information presented as part of this activity is intended solely as
continuing medical education and is not intended to promote off-label
use of any pharmaceutical product. Disclosure of Off-Label Usage: The
dosages of ipratropium and albuterol mentioned in the text are often
greater than the manufacturers recommended doses. These higher doses,
however, have been well-studied in the literature.
Faculty Disclosure: In compliance with all ACCME Essentials, Standards, and
Guidelines, all faculty for this CME activity were asked to complete a full
disclosure statement. The information received is as follows: Dr. Ryan, Dr.
Radeos, Dr. Cydulka, and Dr. Della-Giustina report no significant financial
interest or other relationship with the manufacturer(s) of any commercial
product(s) discussed in this educational presentation.
Accreditation: Mount Sinai School of Medicine is accredited by the
Accreditation Council for Continuing Medical Education to sponsor
continuing medical education for physicians.
Credit Designation: Mount Sinai School of Medicine designates this
educational activity for up to 4 hours of Category 1 credit toward the
AMA Physicians Recognition Award. Each physician should claim only
those hours of credit actually spent in the educational activity.
Emergency Medicine Practice is approved by the American College
of Emergency Physicians for 48 hours of ACEP Category 1 credit (per
annual subscription).
Earning Credit: Two Convenient Methods
Print Subscription Semester Program: Physicians with current and valid
licenses in the United States who read all CME articles during each
Emergency Medicine Practice six-month testing period, complete the
post-test and the CME Evaluation Form distributed with the December
and June issues, and return it according to the published instructions
are eligible for up to 4 hours of Category 1 credit toward the AMA
Physicians Recognition Award (PRA) for each issue. You must complete
both the post-test and CME Evaluation Form to receive credit. Results
will be kept confidential. CME certificates will be delivered to each
participant scoring higher than 70%.
Online Single-Issue Program: Physicians with current and valid licenses
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article and complete the post-test and CME Evaluation Form are
eligible for up to 4 hours of Category 1 credit toward the AMA
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kept confidential. CME certificates may be printed directly from the
Web site to each participant scoring higher than 70%.
64. Which of the following best describes the role of

antibiotics in acute exacerbations of COPD?
a. They are best reserved for patients with pneumonia proven by chest x-ray.
b. They should be used routinely as prophylaxis
during acute exacerbations.
c. They are beneficial when increased dyspnea,
sputum volume, and purulence are present.
d. Simple antibiotics such as amoxicillin, doxycycline,
or trimethoprim-sulfamethoxazole should not be
prescribed.
Class Of Evidence Definitions

Each action in the clinical pathways section of Emergency
Medicine Practice receives an alpha-numerical score based on
the following definitions.
Class I
Always acceptable, safe
Definitely useful
Proven in both efficacy and
effectiveness
Level of Evidence:
One or more large prospective
studies are present (with
rare exceptions)
High-quality meta-analyses
Study results consistently
positive and compelling
Class II
Safe, acceptable
Probably useful
Level of Evidence:
Generally higher levels
of evidence
Non-randomized or retrospective studies: historic, cohort, or
case-control studies
Less robust RCTs
Results consistently positive
Class III
May be acceptable
Possibly useful
Considered optional or
alternative treatments
Level of Evidence:
Generally lower or intermediate levels of evidence
Case series, animal studies,

consensus panels
Occasionally positive results
Indeterminate
Continuing area of research
No recommendations until
further research
Level of Evidence:
Evidence not available
Higher studies in progress
Results inconsistent,
contradictory
Results not compelling
Significantly modified from: The

Emergency Cardiovascular Care
Committees of the American Heart
Association and representatives
from the resuscitation councils of
ILCOR: How to Develop EvidenceBased Guidelines for Emergency
Cardiac Care: Quality of Evidence
and Classes of Recommendations;
also: Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring
effectiveness of community-wide
emergency cardiac care. JAMA
1992;268(16):2289-2295.
Publisher: Robert Williford. Vice President/General Manager: Connie Austin.

Executive Editor: Heidi Frost.
Direct all editorial or subscription-related questions to EB Practice, LLC:

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Emergency Medicine Practice (ISSN 1524-1971) is published monthly (12 times per year)
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constitute endorsement. This publication is intended as a general guide and is
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highly technical and complex subject and should not be used for making specific
medical decisions. The materials contained herein are not intended to establish policy,
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Emergency Medicine Practice is not affiliated

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or medical device manufacturer.
20
April 2002

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EMERGENCY MEDICINE PRACTICE

Acute Exacerbations Of COPD:

Critical Appraisal Of The Literature

Stephen A. Colucciello, MD, FACEP,

Center School of Medicine,

Statistics are like a bikini: what they reveal is suggestive,

Emergency Medicine, Morristown

Upon completing this article, you should be able to:

Date of original release: April 1, 2002.

Medical Service, Orlando, FL.

mostly directed toward the primary care provider and is

Table 1. GOLD Classification Of COPD By Severity.

FEV1/FVC < 70%

II: Moderate COPD

FEV1/FVC < 70%

III: Severe COPD

FEV1/FVC < 70%

* Respiratory failure: PaO2 < 8.0 kPa (60 mmHg) with or

Emergency Medicine Practice

parenchyma, leading to loss of lung elasticity. Once the

among women as well as the fact that women may be more

In the ED, it is important to distinguish between mimics of

In industrialized countries, smoking is the leading cause of

Congestive Heart Failure

Emergency Medicine Practice

should not be used to exclude a dangerous condition.) (See

include advanced age, recent trauma or surgery, prior

Acute Coronary Syndrome

Key Points In COPD

Emergency Medicine Practice

167 patients with no prior history of COPD who presented

dyspneic patient, especially in those with a history of

I have every sympathy with the American who was

Always take an emergency leisurely.Chinese proverb

Emergency Department Evaluation

Emergency Medicine Practice

chest (no wheezes or rales in the presence of respiratory

Do you ever forget to take your medications? Show me

Past Medical History

Emergency Medicine Practice

equally concerning as it may signal impending respiratory

should not be used to diagnose an acute exacerbation of COPD or

Other Blood Tests

Arterial Blood Gas

Brain Natriuretic Peptide

Emergency Medicine Practice

The electrocardiogram (ECG) is most useful in evaluating

Hypoxemia is the most common underlying

Emergency Medicine Practice

to the traditional (and more difficult) two maximal breaths

patients with asthma, there are only observational data

Some patients with acute exacerbations of COPD benefit

The dosing of albuterol in acute exacerbations of COPD is

Emergency Medicine Practice

Clinical Pathway: Emergency Department Therapy

Upright sitting position (Class indeterminate)

Severe acidosis or severe hypercapnia?

Intubate using RSI technique (Class I-II)

Short-acting -agonist (Class I-II)

O2 saturation 90% despite high-flow O2?

Consider NIV if no contraindications (Class II)

Go to top of next page

Clinical Pathway: Emergency Department Therapy