Approach to the patient with dyspnea

Author
Richard M Schwartzstein, MD
Section Editor
Talmadge E King, Jr, MD
Deputy Editor
Helen Hollingsworth, MD
Last literature review version 18.1: enero 2010 | This topic last updated: septiembre 8, 2009
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INTRODUCTION A consensus statement of the American Thoracic Society defined dyspnea in the
following way [1]:
"Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is
comprised of qualitatively distinct sensations that vary in intensity. The experience derives from
interactions among multiple physiological, psychological, social, and environmental factors, and may
induce secondary physiological and behavioral responses."
The American Thoracic Society (ATS) statement on the mechanisms, assessment, and management of
dyspnea, as well as other ATS guidelines, can be accessed through the ATS web site at
www.thoracic.org/sections/publications/statements/index.html.
Dyspnea, or breathing discomfort, is a common symptom that afflicts millions of patients with pulmonary
disease and may be the primary manifestation of myocardial ischemia or dysfunction. Examination of the
language of dyspnea suggests that this symptom represents a number of qualitatively distinct sensations,
and that the words utilized by patients to describe their breathing discomfort may provide insight into the
underlying pathophysiology of the disease.
The key elements in the evaluation of the patient with acute and chronic dyspnea will be reviewed here
with a pathophysiologic construct to guide thinking about a differential diagnosis for the patient with
dyspnea. The basic physiology of dyspnea is discussed separately. (See "Physiology of dyspnea".)
The majority of patients with chronic dyspnea of unclear etiology have one of four diagnoses [2]:

Asthma

Chronic obstructive pulmonary disease (COPD)

Interstitial lung disease

Myocardial dysfunction
PATHOPHYSIOLOGY Most patients with breathing discomfort can be categorized into one of two
groups: respiratory system dyspnea or cardiovascular system dyspnea. Respiratory system dyspnea
includes discomfort related to disorders of the central controller, the ventilatory pump, and the gas
exchanger, while cardiovascular system dyspnea includes cardiac diseases (eg, acute ischemia, systolic
dysfunction, valvular disorders, pericardial diseases), anemia, and deconditioning. More than one process
may be active in a given patient, and the basic physiology of dyspnea does not always adhere to this
structure; for example, stimulation of pulmonary receptors can result from interstitial inflammation
(respiratory system) or interstitial edema (cardiovascular system). (See "Physiology of dyspnea".)
Nevertheless, this construct offers an organized approach to the patient with dyspnea of unclear etiology.
Respiratory The respiratory system is designed to move air by bulk transport from the atmosphere to
the alveoli, where oxygen is exchanged for carbon dioxide by diffusion across the alveolar-capillary
membrane. Carbon dioxide is then removed from the lungs by bulk transport to the atmosphere. Several
components must be functioning smoothly for this process to occur; derangements in any of these
elements can lead to dyspnea.
Controller The "respiratory controller" determines the rate and depth of breathing via efferent signals
sent to the ventilatory muscles. Factors that stimulate the respiratory centers lead to increased ventilation
and breathing discomfort in a variety of settings; these often are secondary to derangements in other
parts of the system, such as hypoxia or hypercapnia due to ventilation/perfusion mismatching in the gas
exchanger. In addition, drugs such as aspirin (at a toxic dose) or progesterone and conditions such as

pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent of problems
in the ventilatory pump or gas exchanger. Typically, dyspnea associated with stimulation of the respiratory
controller is described as a sensation of "air hunger" or an "urge or need to breathe" [3-5]. (See "Control
of ventilation" and "Physiology of dyspnea".)
To some degree, the breathing pattern may also reflect what are presumed to be attempts by the
controller to reduce breathing discomfort. Thus, patients with severe airflow obstruction generally adapt a
slow, deep breathing pattern to minimize the pleural pressures needed to overcome airways resistance.
Alternatively, patients with interstitial fibrosis or kyphoscoliosis and reduced lung or chest wall compliance
have a characteristic rapid, shallow breathing pattern which minimizes the work needed to expand the
thorax. When the controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation
of air hunger. The increase in respiratory rate in the setting of expiratory flow limitation leads to
hyperinflation, reduced inspiratory reserve, and increased dyspnea. For any given "drive to breathe," lower
tidal volumes are associated with more intense breathing discomfort [4,5].
Ventilatory pump The "ventilatory pump" is comprised of the ventilatory muscles, the peripheral
nerves which transmit signals to them from the controller, the bones of the chest wall to which the
respiratory muscles are connected, the pleura which transforms movement of the chest wall to negative
pressure inside the thorax, and the airways that serve as a conduit for the flow of gas from the
atmosphere to the alveoli and back again. The most common derangements of the ventilatory pump result
in a sense of increased "work of breathing" [6-10].
Neuromuscular weakness (eg, myasthenia gravis, Guillain-Barr syndrome) leads to a condition in which
the patient must exert near maximal inspiratory effort to produce a normal negative pleural pressure [11].
Patients with reduced compliance of the chest wall (eg, kyphoscoliosis) or lungs (eg, interstitial fibrosis)
must perform more work than normal to move air into the lungs. Obstructive lung disease is associated
with increased resistance to flow and, in patients with significant hyperinflation, reduced compliance as
breathing occurs on the stiff portion of the pressure-volume curve of the respiratory system. When
hyperinflation results in an end-inspiratory volume that approximates total lung capacity, patients often
complain of an inability to get a deeper satisfying breath [9]. A sensation of chest tightness may also be
present in patients in whom acute bronchoconstriction is the cause of airflow obstruction [6,7,12,13].
Gas exchanger The "gas exchanger" consists of the alveoli and the pulmonary capillaries across which
oxygen and carbon dioxide diffuse. Most of the common cardiopulmonary disorders leading to dyspnea are
associated with some derangement of the gas exchanger due either to destruction of the diffusing
membrane (eg, emphysema, pulmonary fibrosis) or the imposition of fluid or inflammatory material
between the capillaries and the gas in the alveoli. Diseases affecting the gas exchanger are typically
characterized by hypoxemia, either at rest or with exercise, and by chronic hypercapnia in more severe
cases. These gas exchange abnormalities stimulate the respiratory centers in the brainstem and lead to a
sensation of "air hunger" or an increased urge to breathe.
Cardiovascular The cardiovascular system is designed to move oxygenated blood from the lungs to
metabolically active tissues, and then transport carbon dioxide from the tissues back to the lungs. For this
system to work optimally and avert breathing discomfort, one must have a pump that functions without
generating high pulmonary capillary pressures. There must also be sufficient hemoglobin to carry
oxygen and appropriate enzymes to utilize oxygen in the tissues.
Heart failure Heart failure is a clinical syndrome that can result from any structural or functional
cardiac disorder that impairs the ability of the ventricle(s) to fill with or eject blood. Symptoms of heart
failure fall into two major classes: those due to a reduction in cardiac output (fatigue, weakness) and
those due to increased pulmonary or systemic venous pressure and fluid accumulation (dyspnea, edema,
hepatic congestion, and ascites). When heart failure causes an increase in pulmonary venous pressure, it
can lead to dyspnea either by producing hypoxemia or by stimulating pulmonary vascular and/or
interstitial receptors (eg, unmyelinated J-receptors, also called C-fibers). Causes of heart failure include
ventricular systolic dysfunction, ventricular diastolic dysfunction, and valvular disease. Cardiac tamponade
may also lead to dyspnea by increasing pulmonary vascular pressures. (See "Physiology of dyspnea" and
"Evaluation of the patient with suspected heart failure" and "Cardiac tamponade".)
Anemia Anemia can severely impair oxygen delivery because the bulk of oxygen carried in the blood is
hemoglobin-bound. (See "Structure and function of normal human hemoglobins".) Nevertheless, the exact
mechanism by which anemia produces dyspnea is unknown. To the extent that the local pH of
metabolically active cells decreases due to the inability to sustain aerobic metabolism, there may be

stimulation of "ergoreceptors" which are believed to be located in the muscles and which respond to such
changes in the microenvironment of the cell [14,15]. Anemia also leads to increased cardiac output, which
may necessitate elevated left ventricular volume and pulmonary vascular pressures. However, the quality
of dyspnea is usually quite different in these two clinical situations.
Deconditioning Individuals usually complain of respiratory discomfort when they engage in vigorous
physical activity, even in the presence of a normal cardiovascular and respiratory system and normal
hematocrit. More fit individuals experience less discomfort for any given workload; cardiovascular fitness is
determined by the ability of the heart to increase maximal cardiac output and by the ability of the
peripheral muscles to utilize oxygen efficiently for aerobic metabolism.
In contrast, a sedentary existence reduces fitness and leads to dyspnea, often with seemingly trivial tasks.
It is common for patients with chronic cardiopulmonary disease to assume a sedentary lifestyle in an effort
to avoid breathing discomfort. However, the end result over a span of months to years is that the
individual becomes progressively deconditioned and ultimately may be limited more by poor cardiovascular
fitness than by the underlying disease [16]. Dyspnea due to deconditioning is typically described as
"heavy breathing" or a sense of "breathing more" [8], and with careful questioning, one can determine
that the patient is actually limited by fatigue rather than breathing discomfort.
LANGUAGE OF DYSPNEA When eliciting a history from a patient presenting with a complaint of pain,
clinicians are taught to always inquire about the quality of the pain. As an example, chest pain may mean
very different things if it is described as "sharp," "burning," or "crushing." (see "Management of suspected
acute coronary syndrome in the emergency department" section on Characteristic history and associated
symptoms.) .
In the 1970s and 1980s a number of pain questionnaires were developed [17,18], and studies in which
they were utilized for headache and facial pain demonstrated that clinicians could draw inferences about
the cause of these symptoms depending upon the responses of a given patient [19,20].
The notion that pain is comprised of multiple, qualitatively distinct sensations comes easily to most
clinicians because everyone experiences a range of painful sensations as part of normal living (eg,
headaches, stomach aches, tooth pain, burns, bruises, etc). However, if one has a normal
cardiopulmonary system, the only dyspnea one is likely to experience is that which occurs with heavy
exercise. This makes it more difficult for the average examiner to question a patient with breathing
discomfort in a way that captures the subtleties of asthma, heart failure, COPD, or pulmonary embolism
[21].
Questionnaires The first dyspnea questionnaires were developed in the late 1980s based upon
informal data obtained from patients and the systematic questioning of normal subjects made breathless
by the imposition of a range of respiratory tasks [3]. These tasks including breathing when resistive or
elastic loads were added, when end-expiratory lung volume was changed, when tidal volume was
restricted, or when carbon dioxide was inhaled. In these settings, the sensations of respiratory discomfort
produced by the different causes of dyspnea were different and easily distinguishable.
As a result of these studies, clusters of terms emerged that were allied with one or another of the
respiratory tasks. Similar dyspnea questionnaires were then presented to patients with breathing
discomfort from a variety of cardiopulmonary disorders (table 1) [6-8,22]. Subjects were asked to select
the phrases that best described their breathing discomfort, and distinct clusters again emerged. While
some clusters of phrases were common to a number of disease categories (eg, increased work or effort of
breathing was found with COPD, asthma, and neuromuscular disease), each disease had a relatively
unique set of clusters associated with it.
These data suggested that the physiologic mechanisms responsible for dyspnea in each patient group are
likely to have some elements in common, and some that are unique. Attention to the words that patients
use in describing their breathing discomfort may provide insight into the underlying clinical condition as
well as the basic physiologic mechanisms producing dyspnea.
Research in this area is continuing, and one incompletely resolved issue is the potential role that ethnicity
and cultural context play in influencing an individual's description of dyspnea. Studies using dyspnea
questionnaires in the United States [6,8] and the United Kingdom [8] have demonstrated similar sensory
descriptions across a number of disease states. On the other hand, one study of 32 patients with asthma
found significant differences among African-American and white subjects in their use of descriptors [23].
However, in this investigation, subjects were not given a questionnaire nor were they asked to describe

their breathing discomfort; rather, they offered spontaneous comments about any sensations associated
with inhalation of methacholine. Research confirms the utility of studying the qualities of dyspnea in
different languages [24,25]. The cross-cultural generalizability of specific dyspnea questionnaires is
uncertain.
Using questionnaires Most studies of the language of dyspnea have been performed in patients with
known cardiopulmonary disorders or in normal subjects made breathless under experimental conditions.
These indicate the following (table 2) [21]:

Acute hypercapnia or restricted thoracic motion produces a sensation of "air hunger" [4,5,26].

Acute bronchoconstriction leads to a series of sensations from "chest tightness" to an increased

"effort to breathe" to a sensation of "air hunger" as the degree of obstruction worsens [6-8,12,13]. The
sensation of "tightness" appears to be independent of the work of breathing [27].
One study explored the use of dyspnea questionnaires in evaluating patients receiving treatment for acute
bronchoconstriction [10]. Patients undergoing bronchodilator therapy in an emergency department
reported decreased breathing discomfort in association with relief of their "chest tightness." However, the
sense of increased "effort" to breathe persisted, as did moderate spirometric airflow obstruction.
This study may provide insight into the different components of dyspnea in asthma: chest tightness
relieved by bronchodilators may reflect changes in pulmonary receptor activation as bronchospasm
diminishes, while the effort of breathing relates to ongoing airflow obstruction and/or hyperinflation
remaining due to airways inflammation.
Attention to the use of verbal descriptors in such patients may help the clinician avoid underestimation of
the severity of asthma when objective measurements of lung function are not possible.

Patients with COPD complain of an increased "effort to breathe" as well as a sensation of

"unsatisfying breaths" or a sense that they "cannot get a deep breath" [9].

Heart failure is associated with a sensation of "air hunger" and "suffocation" [6].

Cardiovascular deconditioning is characterized by "heavy breathing" [8].

Prospective studies examining the clinical utility of dyspnea questionnaires are underway. We have had
extensive experience using these tools in patients referred for evaluation of chronic dyspnea and have
found them to be helpful, particularly in patients with more than one cardiopulmonary disorder and in
patients in whom dyspnea appears out of proportion to their underlying lung disease. As an example, a
patient with sarcoidosis who experienced worsening shortness of breath was increasing her dose of oral
corticosteroids on the presumption that her parenchymal disease was flaring, but was found to have
superimposed airways reactivity after she selected "chest tightness" as the phrase that best described her
breathing discomfort. Similarly, a patient with COPD who had significant functional constraints presumed
due to his emphysema was found to be limited primarily by cardiovascular deconditioning when he noted
that his dyspnea with exertion was best described as "heavy breathing." He denied the qualities of
dyspnea most typical of COPD (difficulty moving air in or out of his lungs or a sensation of not being able
to get a deep breath).
ACUTE DYSPNEA Breathing discomfort arising over the course of minutes to hours is due to a
relatively limited number of conditions (table 3). These entities typically have associated symptoms and
signs that provide clues to the appropriate diagnosis, eg, substernal chest pain with cardiac ischemia;
fever, cough, and sputum with respiratory infections; urticaria with anaphylaxis; and wheezing with acute
bronchospasm. However, dyspnea may be the sole complaint and the physical examination may reveal few
abnormalities (eg, pulmonary embolism, pneumothorax). In these cases, attention to historical
information and a review of this limited differential diagnosis are important. (See "Evaluation of the adult
with dyspnea in the emergency department".)
Plasma BNP The symptoms and physical findings of heart failure (HF) can be subtle; however,
establishing HF as the etiology of a patient's dyspnea is extremely important because management will be
altered. With chronic and advanced HF, ventricular cells are recruited to secrete atrial natriuretic peptide
(ANP) and brain natriuretic peptide (BNP) in response to the high ventricular filling pressures. As a result,
the plasma concentrations of both hormones are increased in patients with asymptomatic and
symptomatic left ventricular dysfunction, making them useful diagnostic markers.

With the rapid bedside assay for BNP, most dyspneic patients with HF have values above 400 pg/mL, while
left ventricular dysfunction without exacerbation, pulmonary embolism, and cor pulmonale should be
considered in dyspneic patients with plasma BNP concentrations between 100 and 400 pg/mL (graph
1) [28,29]. The value of plasma BNP and its precursor, N-terminal pro-BNP, in distinguishing HF from other
causes of dyspnea is discussed in detail separately. (See "Evaluation of the patient with suspected heart
failure", section on 'BNP and NT-proBNP' and "Brain natriuretic peptide measurement in left ventricular
dysfunction and other cardiac diseases", section on 'Plasma BNP in heart failure'.)
CHRONIC DYSPNEA The etiology of dyspnea may prove elusive when it develops over weeks to
months. Patients commonly have known cardiopulmonary disease, but symptoms are out of proportion to
demonstrable physiologic impairments. A majority of patients with dyspnea of unclear cause have one of
four etiologies: asthma, COPD, interstitial lung disease, or cardiomyopathy [2].
In one study of 85 patients presenting to a pulmonary unit with a complaint of chronic dyspnea, the initial
impression of the etiology of dyspnea based upon the patient history alone was correct in only 66 percent
of cases [2]. Thus, a systematic approach to these patients is necessary.
History and physical examination As noted above, attention to the quality of the breathing
discomfort often provides clues to the underlying diagnosis:

Chest tightness may be indicative of bronchospasm

A sensation of rapid, shallow breathing may correspond to interstitial disease

A sense of heavy breathing is typical of deconditioning

The history may reveal other valuable clues. The absence of cigarette smoking argues strongly against a
diagnosis of chronic obstructive pulmonary disease. The occupational history may lead to a diagnosis of
asbestosis or hypersensitivity pneumonitis. The presence of specific, reproducible inciting events such as
exposure to fumes or cold air is common with airways hyperreactivity. However, a known chronic
cardiopulmonary disease does not guarantee that the patient's symptoms are due to that condition [16].
The rapidity with which symptoms develop during exercise can also provide useful diagnostic information.
For example, patients who develop acute elevations in pulmonary capillary wedge pressure generally
develop shortness of breath and wheezing within 50 to 100 feet. In contrast, symptoms of exerciseinduced asthma usually are precipitated by more intense activity. (See "Exercise-induced
bronchoconstriction".)
In general, the negative predictive value of absent physical findings is higher than the positive predictive
value for signs obtained from the examination of patients with chronic dyspnea [2].
Laboratory and radiographic testing The initial evaluation following the history and physical
examination should include a hematocrit (to exclude anemia as a contributing factor to respiratory
discomfort), a chest radiograph, spirometry, and oximetry during ambulation at a normal pace over
approximately 200 meters.
The chest radiograph may provide evidence of hyperinflation and bullous disease suggestive of obstructive
lung disease, or changes in interstitial markings consistent with inflammation or interstitial fluid.
Abnormalities of heart size may indicate valvular disease or other cardiac dysfunction. Echocardiography is
reserved for patients in whom the heart is enlarged on chest radiograph or in whom the diagnosis of
chronic thromboembolic disease or pulmonary hypertension is being considered.
Spirometry provides data on airway function and can suggest an underlying "restrictive" abnormality that
could be confirmed with measurement of lung volumes. Complete pulmonary function testing with
assessment of lung volumes and diffusing capacity is generally reserved for individuals in whom interstitial
fibrosis is being considered, in those who have significant declines in oxygen saturation with exercise, or in
those for whom there is a question of ventilatory muscle weakness. (See "Overview of pulmonary function
testing in adults" and "Diffusing capacity for carbon monoxide".)
Computed tomography (CT) of the chest usually is not indicated in the initial evaluation of patients with
dyspnea, but can be valuable in three circumstances:

A small percentage of patients with pulmonary fibrosis may have a normal chest radiograph on
presentation; CT scan clearly is more sensitive for detecting mild degrees of alveolitis [30,31]. Thus,
patients with crackles on physical examination or reduced lung volumes on pulmonary function testing
should have CT scans if the chest radiograph is normal.

A minority of patients with a history of cigarette smoking, normal spirometry, and normal chest
radiographs have extensive emphysema on high-resolution CT scan [32]. These patients generally
demonstrate oxygen desaturation with exercise and have a low diffusing capacity.

In patients in whom chronic thromboembolic disease is a consideration due to elevation of

pulmonary artery pressure on an echocardiogram or oxygen desaturation during exercise.
Cardiopulmonary exercise testing Cardiopulmonary exercise testing is indicated when the etiology
of a patient's dyspnea remains unclear after the initial evaluation described above, or when it seems out of
proportion to the severity of the patient's known cardiac or pulmonary disease. This testing, during which
a range of physiologic parameters is monitored, allows one to determine if the patient's dyspnea is more
likely due to cardiovascular or respiratory system abnormalities. (See "Functional exercise testing:
Ventilatory gas analysis" and "Exercise physiology".)
Cardiopulmonary exercise testing is particularly helpful in establishing the diagnosis of deconditioning and
can yield clues about the presence of primary hyperventilation syndromes. The technique also detects
patients with a low threshold for respiratory discomfort; these individuals terminate the test at mild
workloads because of dyspnea but have no evidence of cardiopulmonary abnormality.
BEHAVIORAL CONSIDERATIONS A symptom is the end result of a sequence of events that begins
with stimulation of one or more receptors, leads to the transmission of neural information from those
receptors to the brain, and ultimately involves the processing of that information so that it becomes a
perception. An individual's education, experience, and behavioral style are important in shaping the
ultimate perception of a given stimulus [33,34].
The global rating that a patient gives for dyspnea may reflect both sensory and emotional (ie, affective)
elements. In a study of laboratory-induced dyspnea, air hunger was associated with greater
unpleasantness for a given level of sensory intensity than was the sense of respiratory work or effort [35].
The context in which a sensation occurs may alter the affective component of the intensity and needs to
be considered when assessing the patient.
For a given physiologic derangement, eg, a drop in FEV1 or PaO2, there is a wide range of perceptual
responses among individuals. Anxiety, anger, pain, and depression may be associated with dyspnea
intensity out of proportion to the physiologic impairment [36-39]. Increased ventilation associated with
anxiety, anger or pain may push an individual with a limited pulmonary reserve at baseline closer to his or
her ventilatory limits and increase respiratory discomfort for any given activity.
SUMMARY AND RECOMMENDATIONS Dyspnea can be the first manifestation of a variety of
cardiopulmonary disorders. We recommend the following approach when evaluating a patient with
dyspnea of unclear etiology or dyspnea out of proportion to known physiologic abnormalities:

When developing a differential diagnosis, use a construct that distinguishes respiratory system
dyspnea from cardiovascular dyspnea. It is not uncommon for a patient to have more than one problem
contributing to the breathing discomfort. The most common causes of chronic dyspnea are asthma,
COPD, interstitial lung disease, and cardiomyopathy, but deconditioning is often a major contributing
factor in patients with chronic lung disease (see 'Pathophysiology' above).

Inquire about the quality of the patient's breathing discomfort and attempt to ascertain whether
the individual has more than one type of discomfort under different conditions. Use of dyspnea
questionnaires can be helpful in eliciting this information from patients with chronic dyspnea (see
'Language of dyspnea' above).

Plasma brain natriuretic peptide (BNP) levels may be helpful in establishing or excluding the
diagnosis of heart failure as a cause of acute dyspnea (see 'Acute dyspnea' above).

The history and physical examination lead to accurate diagnoses in patients with dyspnea in
approximately two-thirds of cases; chest radiography and pulmonary function testing should be the first
tests obtained in the majority of cases in which additional information is required. CT scanning is
generally reserved for patients in whom there is a suspicion of interstitial lung disease, occult
emphysema, or chronic thromboembolic disease. (See 'Laboratory and radiographic testing' above.)

Cardiopulmonary exercise testing is a useful study in patients in whom the cause of their breathing
discomfort remains elusive after standard testing, in patients in whom deconditioning is a serious

consideration, and in patients who appear to have breathing discomfort out of proportion to their
physiologic derangements. (See 'Cardiopulmonary exercise testing' above.)
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Evaluation of the adult with dyspnea in the emergency department

Authors
Azeemuddin Ahmed, MD, FACEP
Mark A Graber, MD, FACEP
Eric W Dickson, MD, MHCM, FACEP
Section Editor
Robert S Hockberger, MD, FACEP
Deputy Editor
Jonathan Grayzel, MD, FAAEM
Last literature review version 18.1: enero 2010 | This topic last updated: septiembre 21, 2009
(More)
INTRODUCTION Dyspnea is the perception of an inability to breathe comfortably [1]. The adult
patient with acute dyspnea presents difficult challenges in diagnosis and management. The emergency
clinician must work through a wide differential diagnosis while providing appropriate initial treatment for a
potentially life-threatening illness. Airway, breathing, and circulation are the emergency clinician's primary
focus when beginning management of the acutely dyspneic patient. Once these are stabilized, further
clinical investigation and treatment can proceed.
For the purpose of this review, we will use the term "dyspnea" to encompass all patients with disordered
or inadequate breathing. This topic review will provide a differential diagnosis of the life-threatening and
common causes of dyspnea in the adult, describe important historical and clinical findings that can help to
narrow the differential diagnosis, discuss the use of common diagnostic studies, and provide
recommendations for initial management and disposition. Detailed discussions of specific diagnoses are
found elsewhere in the program.
PATHOPHYSIOLOGY The respiratory system is designed to maintain homeostasis with respect to gas
exchange and acid-base status. Derangements in oxygenation as well as acidemia lead to breathing
discomfort. The development of dyspnea is a complex phenomenon generally involving stimulation of a
variety of mechanoreceptors throughout the upper airway, lungs, and chest wall, and chemoreceptors at
the carotid sinus and the medulla. The pathophysiology of dyspnea is discussed in detail elsewhere. (See
"Physiology of dyspnea" and "Oxygenation and mechanisms of hypoxemia".)
EPIDEMIOLOGY Dyspnea is a common chief complaint among patients who come to the emergency
department (ED). A chief complaint of dyspnea or shortness of breath made up 3.5 percent of the more
than 115 million visits to United States EDs in 2003. Other dyspnea-related chief complaints (cough, chest
discomfort) comprised 7.6 percent [2].
According to one prospective observational study, the most common diagnoses among elderly patients
presenting to an ED with a complaint of acute shortness of breath and manifesting signs of respiratory
distress (eg, respiratory rate >25, SpO2 <93 percent) are decompensated heart failure, pneumonia,
chronic obstructive pulmonary disease, pulmonary embolism, and asthma [3].
DIFFERENTIAL DIAGNOSIS A table listing life-threatening and common causes of dyspnea that
present to the emergency department is provided (table 1).
Life-threatening upper airway causes

Tracheal foreign objects Common objects include food, coins, bones, dentures, medication
tablets, and a multitude of other objects that can be placed in the mouth and become lodged in the
upper and lower airways. This is an uncommon cause of acute dyspnea in adults. (See "Airway foreign
bodies in adults".)

Angioedema Angioedema can cause significant swelling of the lips, tongue, posterior pharynx,
and most dangerously the larynx over minutes to hours, and may progress to severe dyspnea. The skin
may be erythematous or normal in color, but is usually not pruritic. Although first described over a
century ago, the pathophysiology, origin, and treatment of angioedema are not completely understood.
The various types include allergic, NSAID-induced, ACE-inhibitor induced, and complement-related (C1-

esterase inhibitor deficiency or a nonfunctional allele). (See "Treatment of acute attacks in hereditary
and acquired angioedema" and "An overview of angioedema".)

Anaphylaxis Often triggered by foods, insect bites, and various medications, anaphylaxis may
cause severe swelling of the upper airway and tongue, and possibly airway occlusion. Symptoms and
signs develop over minutes to hours and may include skin and mucosal findings (eg, hives, flushing,
oropharyngeal swelling), respiratory compromise (eg, wheezing, stridor, hypoxia), cardiovascular
compromise (eg, hypotension, tachycardia, syncope), and gastrointestinal complaints (eg, abdominal
pain, vomiting). (See "Anaphylaxis: Rapid recognition and treatment".)

Infections of the pharynx and neck A number of oropharyngeal infections can cause acute
dyspnea [4-7]. Epiglottitis generally presents with rapidly progressive sore throat, dysphagia,
hoarseness ("hot potato" voice), and fever. Although once a predominately pediatric disease, epiglottitis
now occurs more often in adults. Pertussis may present with severe paroxysms of cough, but can be
difficult to diagnose clinically. Deep space infections of the neck, from Ludwig's angina, severe tonsillitis,
peritonsillar abscess, and retropharyngeal abscess, can cause swelling and pain, which may manifest in
part as acute dyspnea. (See "Epiglottitis (supraglottitis): Clinical features and diagnosis" and "Clinical
features and diagnosis of Bordetella pertussis infection in adolescents and adults" and "Deep neck space
infections".)

Airway trauma Blunt or penetrating injuries of the head or neck can cause hemorrhage,
anatomic distortion, and swelling, which can compromise the airway and cause acute dyspnea. Suspect
a larynx fracture in patients complaining of dyspnea in the setting of severe neck pain and dysphonia
following blunt trauma. Patients who have sustained facial burns or smoke inhalation are at risk for
rapidly progressive airway compromise and must be emergently evaluated. Early endotracheal
intubation is often indicated. (See "Penetrating neck injuries" and "Emergency care of moderate and
severe thermal burns in adults" and "Smoke inhalation".)
Life-threatening pulmonary causes

Pulmonary embolism The diagnosis of pulmonary embolism (PE) should be considered in any
patient with acute dyspnea. Risk factors include a history of deep venous thrombosis or pulmonary
embolism, prolonged immobilization, recent trauma or surgery (particularly orthopedic), pregnancy,
malignancy, stroke or paresis, and a personal or family history of hypercoagulability. Presentation varies
widely, but dyspnea at rest and tachypnea are the most common signs. A sizable minority of patients
have no known risk factor at the time of diagnosis. Other embolic phenomenon include fat embolism,
especially after a long bone fracture, and amniotic fluid embolism. (See "Overview of acute pulmonary
embolism" and "Diagnosis of acute pulmonary embolism".)

COPD Exacerbations of chronic obstructive pulmonary disease (COPD) can present with acute
shortness of breath. Most often, a viral or bacterial respiratory infection exacerbates the patient's
underlying illness. Pulmonary emboli may be responsible for up to 25 percent of apparent "COPD
exacerbations" and should be suspected when the patient fails to improve with standard COPD
treatment measures. (See "Management of acute exacerbations of chronic obstructive pulmonary
disease".)

Asthma Asthma exacerbations generally present with dyspnea and wheezing. Signs of severe
disease include the use of accessory muscles, brief fragmented speech, profound diaphoresis, agitation,
and failure to respond to aggressive treatment. Extreme fatigue, cyanosis, and depressed mental status
portend imminent respiratory arrest. (See "Treatment of acute exacerbations of asthma in adults".)

Pneumothorax and pneumomediastinum Any simple pneumothorax can develop into a lifethreatening tension pneumothorax. In addition to trauma and medical procedures (eg, central venous
catheter placement), a number of medical conditions increase the risk for developing a pneumothorax.
(See "General approach to blunt thoracic trauma in adults".)
Risk factors for primary spontaneous pneumothorax include smoking, a family history, and Marfan
syndrome. Patients are generally in their 20s and complain of sudden onset dyspnea and pleuritic chest
pain that began at rest. (See "Primary spontaneous pneumothorax in adults".)
Patients with certain pulmonary diseases (including COPD, cystic fibrosis, tuberculosis, and AIDS patients
with pneumocystis pneumonia) are at risk for secondary spontaneous pneumothorax. (See "Secondary
spontaneous pneumothorax in adults".)

Patients who have sustained chest trauma or who have been coughing vigorously may present with
dyspnea, sharp pleuritic chest pain, and subcutaneous emphysema over the supraclavicular area and
anterior neck from pneumomediastinum associated with a pneumothorax

Pulmonary infection Lung infections such as severe bronchitis or pneumonia can cause shortness
of breath and hypoxia. Productive cough, fever, and pleuritic chest pain are common but insensitive
signs. The onset of dyspnea in these patients is generally not acute unless underlying chronic
pulmonary disease is present. A chest radiograph is generally necessary for diagnosis. (See "Diagnostic
approach to community-acquired pneumonia in adults".)

Noncardiogenic pulmonary edema (Adult Respiratory Distress Syndrome [ARDS]) ARDS can
complicate a wide range of conditions and is characterized by rapidly progressive dyspnea, hypoxia, and
bilateral infiltrates on chest x-ray. It can be difficult to distinguish from acute decompensated heart
failure purely on clinical grounds. Brain natriuretic peptide (BNP) and echocardiography can be helpful
for diagnosis. Potential causes include sepsis, shock, severe trauma, toxic inhalations (aspiration,
thermal injury, anhydrous ammonia, chlorine), infections (Hantavirus, SARS), blood transfusion, and
drug overdose (cocaine, opioids, aspirin). (See "Acute respiratory distress syndrome: Epidemiology;
pathophysiology; pathology; and etiology" and "Acute respiratory distress syndrome: Definition; clinical
features; and diagnosis".)

Direct pulmonary injury A pulmonary contusion or laceration is a possible source for acute
dyspnea in any patient with chest trauma. (See "General approach to blunt thoracic trauma in adults".)

Pulmonary hemorrhage Hemorrhage from an injury or an underlying disease (eg, malignancy,

tuberculosis) can cause acute dyspnea.
Life-threatening cardiac causes

Acute coronary syndrome (ACS) Patients, particularly the elderly, suffering from a myocardial
infarction (MI) may present with dyspnea as their sole symptom. Clinicians are more likely to miss an
MI in the patient whose chief complaint is dyspnea. (See "Criteria for the diagnosis of acute myocardial
infarction".)

Acute decompensated heart failure (ADHF) Symptomatic ADHF can be caused by volume
overload, systolic or diastolic dysfunction, or outflow obstruction (eg, aortic stenosis, hypertrophic
cardiomyopathy, severe systemic hypertension). Myocardial ischemia and arrhythmia are common
precipitants. Symptoms range from mild dyspnea on exertion to severe pulmonary edema requiring
emergent airway management. Common findings include tachypnea, pulmonary crackles, jugular
venous distension, S3 gallop, and peripheral edema. ADHF is among the most common causes of acute
respiratory failure among patients over 65 years. (See "Evaluation of acute decompensated heart
failure".)

Flash pulmonary edema The sudden onset and rapid progression of pulmonary edema can be
caused by ischemia, arrhythmia, or drug overdose.

High output heart failure High output heart failure may be precipitated by a number of
conditions, including severe anemia, pregnancy, Beriberi (thiamine deficiency), and thyrotoxicosis. Signs
may include tachycardia, bounding pulses, a venous hum heard over the internal jugular veins, and
carotid bruits. (See "High-output heart failure".)

Cardiomyopathy The physiologic derangements associated with cardiomyopathy (primarily

dilated cardiomyopathy) may result in pulmonary edema and manifest as dyspnea. Potential causes
include cardiac ischemia, hypertension, alcohol abuse, cocaine abuse, and a number of systemic
diseases (eg, sarcoidosis, systemic lupus erymatosus). (See "Causes of dilated cardiomyopathy".)

Cardiac arrhythmia Cardiac conduction abnormalities, such as atrial flutter, atrial fibrillation,
second and third degree heart block, and tachyarrhythmias (eg, SVT and ventricular tachycardia) can
result in dyspnea. Such abnormalities may stem from underlying disease, including myocardial
ischemia. (See "Overview of the evaluation and management of atrial fibrillation" and "Approach to the
diagnosis of narrow QRS complex tachycardias" and "Approach to the diagnosis and treatment of wide
QRS complex tachycardias".)

Valvular dysfunction Aortic stenosis, mitral regurgitation, or ruptured chordae tendinae can
present with acute dyspnea. A murmur may be appreciable, but the absence of an audible murmur does

not exclude the diagnosis. (See "Valvular heart disease in elderly adults", and see reviews of specific
valvular diseases).

Cardiac tamponade Whether due to trauma, malignancy, uremia, drugs, or infection, cardiac
tamponade can present with acute dyspnea. The classically described findings of hypotension, distended
neck veins, and muffled heart tones suggest the diagnosis, but are often absent. The electrocardiogram
generally shows sinus tachycardia and low voltage, and may uncommonly reveal electrical alternans.
(See "Cardiac tamponade".)
Life-threatening neurologic causes

Stroke Although dyspnea is not the chief complaint of patients with an acute stroke, a number of
respiratory abnormalities may result from a stroke. These include aspiration pneumonia, neurogenic
pulmonary edema, and a number of abnormal respiratory patterns, including apnea, that can lead to
severe hypoxia or hypocapnia. Invasive airway management may be required. (See "Stroke-related
pulmonary complications and abnormal respiratory patterns".)

Neuromuscular disease A number of neuromuscular diseases, including multiple sclerosis,

Guillain-Barr syndrome, myasthenia gravis, and amyotrophic lateral sclerosis, can cause weakness of
the respiratory muscles, leading to acute respiratory failure. (See "Epidemiology, risk factors, and
clinical features of multiple sclerosis in adults" and "Clinical features and diagnosis of Guillain-Barr
syndrome in adults" and "Clinical manifestations of myasthenia gravis" and "Clinical features of
amyotrophic lateral sclerosis".)
Life-threatening toxic and metabolic causes

Poisoning A number of toxins can cause derangements in respiratory function, leading to

dyspnea. Organophosphate poisoning causes an increase in airway sections and bronchospasm.
Petroleum distillates and paraquat can cause respiratory difficulty. (See "Organophosphate and
carbamate poisoning" and "Paraquat poisoning".)

Salicylate poisoning Salicylate overdose leads to stimulation of the medullary respiratory center,
causing hyperventilation and respiratory alkalosis initially, followed by metabolic acidosis. In some
cases, pulmonary edema may occur with severe poisoning. Prominent extrapulmonary signs include
fever, tinnitus, vertigo, vomiting, diarrhea, and in more severe cases mental status changes. (See
"Aspirin poisoning in adults".)

Carbon monoxide poisoning Carbon monoxide is a potentially lethal toxin that impairs
oxygen metabolism. Carbon monoxide poisoning may present with tachypnea and acute dyspnea in
moderate cases, and pulmonary edema in severe cases. Extrapulmonary signs are generally more
prominent and often nonspecific. They can include headache, malaise, chest discomfort, and altered
mental status. (See "Carbon monoxide poisoning".)

Toxin related metabolic acidosis Toxic ingestions, including methanol and ethylene glycol, may
cause a metabolic acidosis and compensatory tachypnea that manifest as respiratory distress and may
lead to respiratory failure. (See "Methanol and ethylene glycol poisoning".)

Diabetic ketoacidosis Diabetic ketoacidosis can cause tachypnea and dyspnea largely from the
body's attempt to correct the metabolic acidosis. Patients with diabetic ketoacidosis give a history of
polyuria, polydipsia, polyphagia, and progressive weakness; signs of severe disease include
hyperventilation, altered mental status, and abdominal pain. (See "Clinical features and diagnosis of
diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults".)

Sepsis Severe sepsis often causes respiratory compromise secondary to tachypnea and
respiratory fatigue, which may stem from underlying pneumonia, compensation for lactic acidosis, or
some other process. (See "Management of severe sepsis and septic shock in adults".)

Anemia Acute anemia from hemorrhage, hemolysis, or production abnormalities may result in
dyspnea due to the lack of oxygen carrying capacity. (See "Approach to the adult patient with anemia".)

Acute chest syndrome Chest pain syndrome is a potentially life-threatening complication of sickle
cell disease. In the United States, it is seen predominantly in the African American population. Patients
generally complain of severe chest pain and acute dyspnea and have a fever, while chest x-ray reveals a
new pulmonary infiltrate. (See "Overview of the clinical manifestations of sickle cell disease" and
"Pulmonary complications of sickle cell disease".)

Miscellaneous causes

Lung cancer Shortness of breath is a common symptom in patients with lung cancer at the time
of diagnosis, occurring in approximately 25 percent of cases. Dyspnea may be due to extrinsic or
intraluminal airway obstruction, obstructive pneumonitis or atelectasis, lymphangitic tumor spread,
tumor emboli, pneumothorax, pleural effusion, or pericardial effusion with tamponade. (See "Overview
of the risk factors, pathology, and clinical manifestations of lung cancer".)

Pleural effusion A pleural effusion, secondary to infection, ascites, pancreatitis, cancer, heart
failure, or trauma, can cause severe acute dyspnea. Analysis of the pleural fluid is often necessary to
determine the source. (See "Diagnostic evaluation of a pleural effusion in adults".)

Intraabdominal processes A number of conditions such as peritonitis, ruptured viscous, or bowel

obstruction can cause severe pain that affects respiration and may manifest as acute shortness of
breath, although this is generally not the patient's primary complaint [8]. (See "Evaluation of the adult
with abdominal pain in the emergency department".)

Ascites Ascites secondary to malignancy or liver disease can distend the abdominal cavity,
placing pressure on the diaphragm and thereby increasing the work of breathing [9]. In such cases,
symptoms often improve after large-volume paracentesis. (See "Diagnosis and evaluation of patients
with ascites".)

Pregnancy A number of physiologic changes occur during pregnancy that effect respiratory
function, including an increase in minute ventilation, a decrease in functional residual capacity, a
decrease in hematocrit, and elevation of the diaphragm. Approximately two-thirds of women experience
dyspnea during the course of normal pregnancy.
However, pregnancy increases the risk for several potentially life-threatening conditions that may manifest
with dyspnea, notably pulmonary embolism. Pulmonary edema may be identified in the setting of a
number of diseases associated with pregnancy, including preeclampsia, amniotic fluid embolism, and
cardiomyopathy. (See "Dyspnea during pregnancy" and "Deep vein thrombosis and pulmonary embolism
in pregnancy: Epidemiology, pathogenesis, and diagnosis" and "Eclampsia" and "Amniotic fluid embolism
syndrome" and "Peripartum cardiomyopathy" and "Management of heart failure in pregnancy".)

Massive obesity Massive abdominal girth can interfere with ventilation, causing dyspnea and
hypoxia. (See "Pathogenesis of obesity hypoventilation syndrome" and "Health hazards associated with
obesity in adults".)

Hyperventilation and anxiety Hyperventilation from anxiety is a diagnosis of exclusion in the

emergency department. Even among young healthy patients with a known anxiety disorder, it is prudent
to perform a history and physical examination to screen for medical causes of dyspnea. To complicate
matters, anxiety is common among patients with severe medical disease. As an example, COPD patients
have a three-fold increase in the prevalence of anxiety disorders compared with the general population
[10]. In such patients, it is best to assume that an exacerbation of their underlying medical disease is
the cause of dyspnea, until proven otherwise.
HISTORY The history is critical to the evaluation of the acutely dyspneic patient, but can be difficult to
obtain when the patient has difficulty speaking and the clinician must concentrate on ensuring that the
patient maintains adequate oxygenation and ventilation. Relevant history can be obtained from the
patient, EMS providers, family and friends, pharmacists, and primary care clinicians. The following details
should be obtained whenever possible:

General historical features Ask about the events leading up to the episode, particularly any
recent symptoms or specific triggers for the acute dyspnea. As examples, noncompliance with
medications or diet may lead to an episode of acute decompensated heart failure (ADHF), exposure to
cold or an allergen may trigger an asthma flare, acute dyspnea immediately following a meal suggests
an allergic reaction, a new productive cough suggests a pulmonary infection, recent surgery or
immobilization increases the risk for pulmonary embolism (PE), while recent trauma may have caused a
pneumothorax or pulmonary contusion.

Past history Determine whether the problem is new or recurring. Ask about preexisting medical
conditions, such as asthma, COPD, or ischemic heart disease, and whether the patient has experienced
similar acute episodes before. If it resembles prior episodes, the current problem is often an

exacerbation of a preexisting illness. The medical record and medication list can provide important
diagnostic clues.

Prior intubation Patients with a history of endotracheal intubation for medical conditions have a
higher risk for severe disease and the need for subsequent intubation. As an example, patients who
have required intubation for a severe asthma exacerbation are at increased risk for subsequent episodes
of near-fatal asthma attacks. (See "Identifying patients at risk for fatal asthma".)

Time course Ask whether the dyspnea developed suddenly or gradually. Keep in mind that
exacerbations of a single illness can present in different ways and over different periods of time. As
examples, an asthma flare may develop over minutes or days, as may episodes of heart failure. A table
is provided to help differentiate causes of respiratory distress based on time course (table 2).

Severity When asked to grade the severity of their distress using a scale of 1 to 10 (1 = just
noticeable, 3 = slight, 5 = moderate, 7 = moderately severe, 9 = very severe and 10 = panic level),
patients with acute exacerbations of asthma, COPD and ADHF tend to rate their distress as moderately
severe (score of 7), while those experiencing dyspnea associated with normal pregnancy,
neuromuscular disorders or PE tend to rate their distress as only moderate (score of 5) [11].

Chest pain Chest pain in association with dyspnea occurs with a number of diseases, including
acute coronary syndrome (ACS), pneumothorax, and PE. Of note, a sizable minority of patients with
ACS or PE complain of dyspnea alone. (See "Evaluation of chest pain in the emergency department".)

Trauma Injury to the airway, neck, chest wall, lungs, heart, mediastinal structures, or abdomen
can lead to dyspnea. Acute symptoms may not manifest until a day or longer following trauma. (See
"General approach to blunt thoracic trauma in adults".)

Fever Fever can be associated with an infection, hypersensitivity pneumonitis, aspiration

pneumonitis, or poisoning. As an example of the latter, aspirin overdose can present with fever and
abnormal breathing. (See "Aspirin poisoning in adults".)

Paroxysmal nocturnal dyspnea (PND) Keep in mind that PND is NOT specific for ADHF. Patients
with COPD may present with a similar history.

Hemoptysis Hemoptysis is associated with a number of diseases, including PE, tuberculosis, and
malignancy, when tumors erode into a vascular structure. (See "Causes and management of massive
hemoptysis in adults".)

Cough and sputum The presence and quality of sputum may be helpful. Purulent sputum
suggests pneumonia and white or pink frothy sputum suggests ADHF, while frankly bloody sputum
suggests infection (eg, tuberculosis) or pulmonary hemorrhage (eg, pulmonary embolism or
malignancy). A nonproductive cough is a nonspecific symptom, and may be associated with asthma,
heart failure, respiratory infection, or PE.

Medications A review of the patient's medications can prove helpful. In addition to information
about chronic or acute illness (eg, recent antibiotic prescription), a medication list may provide
information about recent changes in medications or dosing. It is important to ask about compliance.
Obtaining information directly from the patient's pharmacy can be helpful.

Tobacco and drugs Knowledge of the patient's tobacco and drug use can provide insight into the
differential diagnosis. Tobacco use increases the risk for a number of chronic conditions (COPD,
malignancy), while inhaled drug use can lead to such conditions as crack lung and ARDS.
Noninhalational use or overdose of certain drugs, such as opioids and aspirin, can produce acute lung
injury. (See "Cocaine: Acute intoxication" and "Opioid intoxication in adults" and "Aspirin poisoning in
adults" and "Overview of pulmonary disease in injection drug users".)

Psychiatric conditions Psychogenic causes for acute dyspnea represent diagnoses of exclusion in
the emergency department. Organic causes MUST be thoroughly considered first. Nevertheless, among
patients younger than 40 years with no medical conditions, psychogenic dyspnea (eg, anxiety attack)
may be the cause in a sizable minority of patients [12,13].
PHYSICAL EXAMINATION

Clinical danger signs The emergency clinician should perform a screening physical examination
looking for signs of significant respiratory distress in all patients with acute dyspnea. A brief inspection is
often sufficient for this purpose.
Signs that portend imminent respiratory arrest include:

Depressed mental status

Inability to maintain respiratory effort

Cyanosis
Many patients in respiratory distress appear anxious and sit bolt upright or in a tripod position. They often
breath rapidly, use accessory muscles, and sweat profusely. They may be unable to answer questions with
anything more than a few words. Stridor or wheezing may be audible.
Signs suggestive of severe respiratory distress include:

Retractions and the use of accessory muscles

Brief, fragmented speech

Inability to lie supine

Profound diaphoresis; dusky skin

Agitation or other altered mental status

Retractions occur with airway obstruction (eg, asthma, COPD, foreign body) and can be seen in the
suprasternal, intercostal, and subcostal areas [14]. They are an ominous sign suggesting extreme
respiratory distress. The use of accessory muscles to breathe suggests fatigue of the respiratory muscles
and suggests the potential for respiratory failure.
Diaphoresis reflects extreme sympathetic stimulation associated with severe disease (myocardial
infarction, severe asthma flare). Cyanosis is uncommon and indicates severe hypoxia or
methemoglobinemia.
Altered mental status (eg, agitation or somnolence) in the dyspneic patient suggests severe hypoxia or
hypercarbia. It may also be caused by a toxin (eg, salicylate overdose, carbon monoxide) or underlying
pathology (eg, hypoglycemia, sepsis).
General examination findings Once a screen for clinical danger signs is completed and any
necessary resuscitation is initiated, a more thorough physical examination is performed. Important items
to note are described below and in the accompanying table (table 3). Keep in mind that an unremarkable
pulmonary and cardiac examination does NOT rule out significant disease. As examples, the sensitivity and
specificity of the pulmonary examination are limited for making the diagnosis of pneumonia or ADHF [1519].

Respiratory rate Patients with serious underlying disease may have a fast, normal, or slow
respiratory rate (RR). As an example, patients with a pulmonary embolism may have a RR in the normal
range.

Pulse oximetry Pulse oximetry provides crucial information about arterial oxygenation. However,
clinicians must be aware that standard pulse oximeters are NOT accurate in the setting of hypothermia,
shock, carbon monoxide poisoning, and methemoglobinemia. (See "Pulse oximetry".)
In general, healthy individuals demonstrate an oxygen saturation (SpO2) of 95 percent or greater. Elders
and patients who are obese or smoke heavily often maintain levels between 92 and 95 percent, while
patients with severe chronic lung disease may have baseline levels below 92 percent. In the setting of
acute dyspnea, oxygenation levels lower than expected, or below a patient's known baseline, should be
investigated and explained. A drop in SpO2 associated with exercise is characteristic of Pneumocystis
pneumonia. SpO2 levels before and after exercise should be noted in patients suspected or known to have
HIV. (See "Clinical presentation and diagnosis of Pneumocystis carinii (P. jirovecii) infection in HIV-infected
patients".)

Other vital signs Clinicians must review a complete set of vital signs. Dyspnea and hypotension
are an ominous combination.

Abnormal breath sounds

- Stridor occurs when there is airway obstruction. Inspiratory stridor suggests obstruction above
the vocal cords (eg, foreign body, epiglottitis, angioedema). Expiratory stridor or mixed inspiratory and
expiratory stridor suggests obstruction below the vocal cords (eg, croup, bacterial tracheitis, foreign
body).

- Wheezing suggests obstruction below the level of the trachea and is found with asthma,
anaphylaxis, a foreign body in a mainstem bronchus, acute decompensated heart failure (ADHF), or a
fixed lesion such as a tumor.

- Crackles (rales) suggest the presence of interalveolar fluid, as seen with pneumonia or ADHF.
They can also occur with pulmonary fibrosis. However, the absence of crackles does not rule out the
presence of pneumonia, ADHF, or pulmonary fibrosis [15].

- Diminished breath sounds can be caused by anything that prevents air from entering the lungs.
Such conditions include: severe COPD, severe asthma, pneumothorax, tension pneumothorax, and
hemothorax, among others.

Cardiovascular signs

- An abnormal heart rhythm may be a response to underlying disease (eg, tachycardia in the
setting of PE) or the cause of dyspnea (eg, atrial fibrillation in the setting of chronic heart failure).

- Heart murmurs may be present with acute decompensated heart failure (ADHF) or diseased or
otherwise compromised cardiac valves. (See "Auscultation of heart sounds".)

- An S3 heart sound suggests left ventricular systolic dysfunction, especially in the setting of ADHF.

- An S4 heart sound suggests left ventricular dysfunction and may be present with severe
hypertension, aortic stenosis, hypertrophic cardiomyopathy, ischemic heart disease, or acute mitral
regurgitation.

- Muffled or distant heart sounds suggest the presence of cardiac tamponade, but must be
interpreted in the context of the overall clinical setting.

- Elevated jugular venous pressure may be present with ADHF or cardiac tamponade. It can be
assessed by observing jugular venous distension or examining hepatojugular reflux.

Pulsus paradoxus Pulsus paradoxus can occur when right heart function is compromised, such as
can be seen with severe asthma, pulmonary embolism, or cardiac tamponade. (See "Pulsus paradoxus
in pericardial disease".)
Under normal conditions, inspiration increases systemic venous return and right heart volumes increase;
the free wall of the right ventricle expands into the unoccupied pericardial space with little impact on left
heart volume.
When the contents of the pericardial sac acutely increase, due to the accumulation of pericardial fluid or
with cardiac dilatation, the effective compliance of all chambers becomes that of the tightly-stretched
pericardium. As a result, the increase in right heart filling that occurs during inspiration can only be
accommodated by a bowing of the interventricular septum toward the left heart. This leads to a reduction
in left ventricular diastolic volume, a lower stroke volume, and a consequent decrease in systolic pressure
during inspiration
In order to determine if a pulsus paradoxus is present, measure the patient's systolic blood pressure after
a normal exhalation. Then have the patient inhale normally and determine systolic pressure when the
lungs are expanded. Pulsus paradoxus exists if the difference in systolic pressures is greater than 10
mmHg. Keep in mind that the absence of pulsus paradoxus does not rule out any disease.

Inspection Examine the skin for discoloration suggesting hypoxia or poor perfusion, signs of an
allergic reaction, and evidence of trauma.

Extremities Peripheral edema may not occur with acute left heart failure, but if present suggests
ADHF as the cause of dyspnea. Clubbing is associated with conditions causing chronic hypoxemia.
ANCILLARY STUDIES

General approach Ancillary testing should be performed in the context of the history and examination
findings. Random testing without a clear differential diagnosis can mislead the clinician and delay
appropriate management. The use of dyspnea biomarker panels does not appear to improve accuracy
beyond clinical assessment and focused testing [20,21]. Nevertheless, a chest x-ray and an
electrocardiogram are obtained in most emergency department (ED) patients with acute dyspnea.
Chest x-ray (CXR) A CXR is obtained for most ED patients with acute dyspnea. Particularly when
abnormalities are identified, it is useful to compare the radiograph to past studies.

Acute heart failure Signs of ADHF that may appear on a CXR include: cardiomegaly,
cephalization of blood vessels, interstitial edema (eg, "Kerley B" lines, peribronchial cuffing), and
vascular congestion. Pleural effusions may be present. Keep in mind that the radiograph may lag behind
the clinical picture and approximately 20 percent of patients admitted with ADHF have a nondiagnostic
CXR [22]. (See "Evaluation of the patient with suspected heart failure".)

Pneumonia Although an infiltrate on CXR is considered the "gold standard" for diagnosing
pneumonia, radiographs obtained early in the clinical course may be nondiagnostic [23]. Volume
depletion may also lead to a negative initial CXR. Contrary to past teaching, the appearance of the CXR
does not accurately predict the nature of the pneumonia. (See "Diagnostic approach to communityacquired pneumonia in adults".)

Pneumothorax A pneumothorax sufficient to cause acute dyspnea is usually visible on CXR. An

expiratory view may be helpful [24]. Patients in extremis with a suggestive history and examination
findings consistent with a tension pneumothorax should be treated with immediate needle
decompression before obtaining a CXR. (See "Imaging of pneumothorax".)

COPD and asthma Large lung volumes and a flattened diaphragm on CXR suggest air trapping,
which occurs with COPD or asthma. Unilateral air trapping suggests a foreign body. Many patients with
mildly or moderately severe COPD and most patients with asthma have an unremarkable CXR. (See
"Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging" and
"Treatment of acute exacerbations of asthma in adults".)
Electrocardiogram An electrocardiogram (ECG) with ST segment deviations constitutes strong
evidence supporting the diagnosis of cardiac ischemia. However, emergency clinicians must remember that
neither normal biomarkers nor a nondiagnostic ECG can rule out cardiac disease in the ED. The initial ECG
is normal in approximately 20 percent of patients subsequently diagnosed with a myocardial infarction,
and only 33 percent of initial ECGs are diagnostic. The ECG may also reveal signs of pulmonary embolism
(right heart strain), pericardial tamponade (diffuse low voltage, electrical alternans), and other disease
processes. It is helpful to compare the ECG to prior studies. (See "Criteria for the diagnosis of acute
myocardial infarction" and "Diagnosis of acute pulmonary embolism" and "Diagnosis and treatment of
pericardial effusion".)
Cardiac biomarkers Elevated biomarkers support the diagnosis of cardiac ischemia. However, the
initial cardiac biomarkers (troponin I and CK-MB) obtained in the ED are frequently normal. Serial
measurements of cardiac biomarkers are necessary to rule out an acute coronary syndrome. Cardiac
biomarkers have limited specificity and may be elevated in the setting of pulmonary embolism, sepsis,
pericarditis, myocarditis, warfarin use, renal failure, and interference with the assay (generally from
monoclonal antibodies or rheumatoid factor). (See "Troponins and creatine kinase as biomarkers of cardiac
injury" and "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".)
Brain natriuretic peptide The measurement of brain natriuretic peptide (BNP) may be helpful when
the diagnosis of acute decompensated heart failure (ADHF) is in question. BNP testing is not helpful when
used indiscriminately in patients with acute dyspnea [25].
A BNP of less than 100 pg/mL has a negative predictive value of over 90 percent for ADHF. Likewise, a
BNP above 500 pg/mL strongly suggests ADHF, with a positive predictive value over 90 percent. A level
between 100 pg/mL and 500 pg/mL cannot differentiate between ADHF and other causes of elevated BNP.
Causes of a false positive BNP (generally between 100 pg/mL and 500 pg/mL) include pulmonary
embolism, fluid overload states (renal failure, liver failure), critical illness, and other causes of right
ventricular distension (cor pulmonale, pulmonary hypertension). (See "Brain natriuretic peptide
measurement in left ventricular dysfunction and other cardiac diseases".)
D-Dimer Use of the d-dimer depends upon the patient's pretest probability for PE. Patients at low risk
for PE according to a validated scoring system (eg, modified Wells criteria for PE) and a negative ELISA d-

dimer can be ruled out for PE without further testing. It is NOT appropriate to use a d-dimer to screen
patients at higher risk for thromboembolic disease. Patients with malignancy or recent surgery and elderly
patients are more likely to have a falsely elevated d-dimer. (See "Diagnosis of acute pulmonary
embolism".)
Arterial blood gas The role of the arterial blood gas (ABG) in the diagnosis and treatment of the
acutely dyspneic patient is limited. Oxygenation is easily assessed using transcutaneous pulse oximetry.
Acid-base status can be assessed using a venous blood gas and the serum bicarbonate. (See "Arterial and
mixed venous blood gases in lactic acidosis".)
An ABG may be useful in the assessment of the patient presumed to be somnolent from CO2 retention. In
many patients the presence of CO2 retention can be determined using end-tidal CO2 monitors. The PaCO2
should be low in the acutely dyspneic patient, who is usually hyperventilating.
Carbon dioxide monitoring Capnography (ie, end-tidal CO2) provides dynamic monitoring of
ventilatory status in patients with acute respiratory distress. By measuring end-tidal CO2 and respiratory
rate with each breath, capnography provides instantaneous feedback on the clinical status of the patient,
while trends enable the clinician to determine whether the patient's ventilation is worsening despite
treatment (increasing EtCO2), stabilizing (stable EtCO2), or improving (decreasing EtCO2). (See "Carbon
dioxide monitoring (capnography)".)
Chest CT and VQ scan A multidetector computed tomography (MDCT) scan of the chest can be used
to diagnose multiple problems, including PE, malignancy, pneumonia, and pulmonary edema. Often these
diseases can be diagnosed by history, examination, and basic testing, without the use of MDCT. MDCT
entails risk for several complications, including contrast-induced nephropathy, allergic reaction to contrast,
and radiation, and should be used with discretion. Ventilation-perfusion scanning is an alternative method
for diagnosing PE in patients unsuitable for MDCT.
Peak flow and pulmonary function tests (PFTs) The peak expiratory flow rate (PEFR) can be
helpful in distinguishing pulmonary and cardiac causes of dyspnea and determining the severity of
bronchoconstriction in cases of severe asthma. Normal values vary with gender, height, and age, and
accuracy depends upon patient cooperation.
Small observational studies suggest PEFR is generally higher in patients with a cardiac cause of dyspnea
[26,27]. During acute asthma exacerbations, PEFR measurements provide a screening tool for the
presence of hypercapnia and obviate the need for routine arterial blood gases. In the absence of
respiratory depressant medications (eg, narcotics or sedatives), hypercapnia occurs only when the PEFR
falls below 25 percent of normal. Bedside spirometry is less prone to error but may be difficult to perform
in the ED. (See "Peak expiratory flow rate monitoring in asthma" and "Overview of pulmonary function
testing in adults".)
Negative inspiratory force Negative inspiratory pressure (NIF) and forced vital capacity
measurements can be obtained at the bedside to assess dyspneic patients with possible neuromuscular
disease (eg, myasthenia gravis, Guillain-Barr) or musculoskeletal disease (ankylosing spondylitis, severe
scoliosis, or kyphosis). If the NIF is less than 30 cm H2O or the forced vital capacity (FVC) is less than 20
mL/kg, the patient should be admitted to an intensive care unit in anticipation of the need for mechanical
ventilation [28]. These numbers are guidelines only and do not always predict which patients need
respiratory support. (See "Tests of respiratory muscle strength".)
MANAGEMENT
Initial interventions and differential diagnosis For any patient with acute severe dyspnea, the
following measures are performed immediately:

Oxygen is provided

Intravenous access is established and blood obtained for laboratory measurements

Cardiac and pulse oximetry monitoring is instituted

Airway management equipment is brought to the bedside

A screening examination, including an assessment of airway difficulty and a search for rapidly
reversible causes (tension pneumothorax, pericardial tamponade, upper airway foreign body) is
performed. (See "The difficult airway in adults".)

Bedside ultrasound can be of great benefit in determining the presence of pneumothorax or tamponade.
Common life-threatening causes of dyspnea to be considered in all cases include:

Acute coronary syndrome

Acute heart failure

Arrhythmia

Pericardial tamponade

Pulmonary embolism

Pneumonia or other infection

COPD exacerbation

Asthma

Angioedema and anaphylaxis

Poisoning (eg, carbon monoxide)

Trauma (eg, pneumothorax, hemothorax)

A more complete list of potential diagnoses is provided above. (See 'Differential diagnosis' above.)
Emergent management Three primary goals exist for the emergency clinician faced with an acutely
dyspneic patient:

Optimize arterial oxygenation

Determine the need for emergent airway management and ventilatory support

Establish the most likely causes of dyspnea and initiate treatment

The initial decision to provide noninvasive or invasive ventilatory support is made based upon clinical
grounds, not laboratory values. Emergent airway management is discussed in detail elsewhere. (See "The
decision to intubate" and "Rapid sequence intubation in adults" and "The difficult airway in adults" and
"Emergent surgical cricothyroidotomy (cricothyrotomy)".)
Oxygen is a potent and readily available treatment for many causes of dyspnea and should be
administered liberally. For patients with mild dyspnea and normal room-air arterial oxygen saturation
(SpO2), 2 liters per minute (LPM) of oxygen via nasal cannula is typically adequate. For hypoxic patients
with respiratory difficulty, 50 to 60 LPM of oxygen should be provided via a nonrebreather mask. To deliver
this much oxygen, open the flow meter valve until the indicator lies well beyond the 15 LPM mark.
Patients breathing 100 percent oxygen deliver five times as much oxygen to the alveoli per unit of
ventilation as those breathing room air and in the absence of parenchymal disease can maintain a normal
SpO2 with only 2 or 3 breaths per minute. Note, however, that the best nonrebreather oxygen delivery
systems provide only 85 percent oxygen.
Do NOT withhold oxygen from patients with COPD. The target oxygen saturation in such patients is 90 to
94 percent with the understanding that this may result in hypercarbia and reduce ventilatory drive. If a
clinician determines that a COPD patient requires endotracheal intubation, oxygen delivery should be
maximized without regard for the target oxygen saturation or hypercarbia. (See "Management of acute
exacerbations of chronic obstructive pulmonary disease" and "Use of oxygen in patients with
hypercapnia".)
While oxygen is provided and initial interventions (eg, IV access) are made, the clinician determines the
need for airway management and ventilatory support. For patients that require ventilatory assistance to
overcome an infraglottic challenge (eg, bronchospasm or parenchymal disease) or nonpulmonary disease
(eg, neuromuscular disease), both noninvasive and invasive strategies exist. Noninvasive ventilation with a
mask delivering continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BLPAP)
can increase minute ventilation, reduce the work of breathing, recruit alveoli, and improve hemodynamics.
Noninvasive ventilation improves outcomes in patients with acutely decompensated heart failure (ADHF)
or a COPD exacerbation. (See "Noninvasive positive pressure ventilation in acute respiratory failure in
adults" and "Treatment of acute decompensated heart failure".)

Noninvasive ventilation does NOT improve outcomes in patients with acute exacerbations of asthma and
diseases that do not respond rapidly to medical therapy (eg, pneumonia and ARDS). In such instances,
endotracheal intubation and controlled mechanical ventilation should be pursued aggressively when
ventilatory support is needed. (See "Treatment of acute exacerbations of asthma in adults" and
"Treatment of community-acquired pneumonia in adults who require hospitalization" and "Supportive care
and oxygenation in acute respiratory distress syndrome" and "Mechanical ventilation in the emergency
department".)
As with all life-threatening complaints, dyspnea is managed by clinicians performing therapeutic
interventions and diagnostic assessment concurrently. Often therapy assists in diagnosis. As examples, an
improvement in SpO2 immediately after the administration of low-flow oxygen indicates a ventilationperfusion (V/Q) mismatch, while rapid improvement following treatment with bronchodilators strongly
suggests bronchoconstriction. (See "Oxygenation and mechanisms of hypoxemia".)
An electrocardiogram (ECG) and stat portable chest x-ray (CXR) should be obtained early in the course of
management. The ECG may reveal signs of cardiac ischemia, such as ST segment deviations or inverted T
waves. Findings of right heart strain (eg, inverted T waves in the right precordial or inferior leads,
complete or incomplete right bundle branch block, right axis deviation) are consistent with pulmonary
embolism (PE). Diffuse low voltage or electrical alternans in a patient with dyspnea and hypotension
suggests pericardial tamponade. (See 'Electrocardiogram' above and "Criteria for the diagnosis of acute
myocardial infarction" and "Diagnosis of acute pulmonary embolism".)
A portable CXR may reveal cardiomegaly and other signs of pulmonary edema, a pneumothorax,
hyperinflated lungs with flattened diaphragms suggestive of COPD, or an infiltrate suggestive of
pneumonia. Nevertheless, many life-threatening causes of dyspnea may not manifest any abnormality on
CXR. Bedside ultrasound can be useful in making the diagnosis of pneumothorax or pericardial
tamponade. (See 'Chest x-ray (CXR)' above.)
Clinicians should take care not to confuse pneumonia and ADHF, which can have a similar appearance on
CXR and sound similar with auscultation. Blood pressure, treatment response, and brain natriuretic
peptide (BNP) can help to distinguish the two. Pneumonia is more often associated with a normal or low
blood pressure, does not respond to early therapy, and is generally NOT associated with a rise in BNP.
ADHF is generally associated with a high blood pressure, often responds to aggressive early therapy, and
is associated with a rise in BNP. (See 'Brain natriuretic peptide' above.)
The diagnosis of PE can be difficult to make. Although most patients with dyspnea secondary to a PE
demonstrate some abnormality on CXR or ECG, there are no pathognomonic findings in either test. A
definitive diagnosis is made based upon imaging with a multidetector CT or ventilation perfusion scan.
Although obvious causes of dyspnea are treated as they are identified, in some instances the cause of
dyspnea is not immediately apparent. In such cases, the ED clinician must intervene with treatments or by
obtaining emergent consultation based upon the clinical context and available data. As examples, such
interventions may include broad spectrum antibiotics when infection is suspected or stress dose
glucocorticoids for patients who use such medications chronically.
When managing a life-threatening complaint with a broad differential diagnosis such as severe, acute
dyspnea, it is crucial that emergency clinicians not fall prey to premature diagnostic closure. Clinical,
laboratory, and radiographic findings that contradict the clinicians initial impressions must be carefully
considered.
Nonemergent management In most instances, the emergency clinician can determine the diagnosis
or the need for hospital admission based upon a thorough history, physical examination, chest radiograph,
and electrocardiogram. Close attention should be paid to the patient's history of present illness,
comorbidities, vital signs, oxygen saturation, and examination of the airway, lungs, and cardiovascular
system.
Common, potentially life-threatening causes of dyspnea should be considered in all cases. These are listed
above. (See 'Initial interventions and differential diagnosis' above.)
Often the cause of dyspnea cannot be determined with certainty in the ED. In such cases, the clinician's
job is to treat and appropriately triage the patient based upon the clinical scenario and an assessment of
the patient's risk. High risk dyspneic patients include the elderly and those who are immunocompromised,
have severe underlying lung or heart disease, or demonstrate unexplained abnormal vital signs.

DISPOSITION The patient's condition, preliminary diagnosis, and risk assessment determine
disposition. Patients with severe disease or those at risk of rapid deterioration who require close
monitoring should be admitted to an intensive care setting. Those with less severe disease but who fail to
improve with treatment in the ED or who have significant comorbidities or risk factors are admitted to the
appropriate hospital ward.
Stable patients whose evaluation has ruled out significant disease or determined that the risk for such
disease is acceptably low may be discharged. Patients being discharged must have a clear understanding
of their discharge diagnosis, written discharge instructions, and planned follow-up with clear instructions
to return to the ED if their condition worsens. Particularly with elderly patients, the clinician must consider
such factors as the patient's living situation and access to medical follow-up when determining the
appropriateness of discharge.
PITFALLS IN MANAGEMENT

Failure to secure the airway in a timely manner.

Failure to recognize and act on abnormal vital signs and signs of impending respiratory failure.

Over-reliance upon a single finding (physical examination or test result) to establish a diagnosis.

Failure to generate a proper differential diagnosis (ie, premature diagnostic closure).

Failure to monitor the patient's clinical course.

Failure to consider CO poisoning or pulmonary embolism.

Misinterpreting tachypnea, which may not represent a respiratory abnormality and may reflect
nonpulmonary disease (eg, metabolic acidosis or impending herniation of the brainstem).

Allowing patients with a tenuous respiratory status to leave the ED and deteriorate in the radiology
suite.

Discharging patients with inadequate follow-up or unclear instructions.

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