Prim Care Clin Office Pract

33 (2006) 643–657

Evaluation of the Dyspneic

Patient in the Office
Saiyad Sarkar, MD, Pamela J. Amelung, MD*
Division of Pulmonary and Critical Care Medicine, Department of Medicine,
University of Maryland School of Medicine, 10 N. Greene Street 3D-122,
Baltimore, MD 21201, USA

Dyspnea literally means disordered breathing. It is a term generally ap-

plied to the sensations experienced by individuals who complain of unpleas-
ant or uncomfortable respiratory sensations. Dyspnea occurs in healthy
individuals (ie, with exercise or at high altitude), but respiratory patients ex-
perience dyspnea at lower levels of exercise or altitude. Dyspnea may be
considered part of the warning system for humans to recognize when they
are at risk of receiving inadequate ventilation. Dyspnea has been shown
to be an independent predictor of mortality [1], and has been found to be
related to quality of life more than pulmonary function tests [2]. A precise
or widely accepted definition of dyspnea does not exist, because patients
use an array of terms to describe their breathing sensation, and the term
dyspnea represents a number of qualitatively distinct sensations. The specific
descriptive words used by patients to describe their breathing may provide
insight into the underlying pathophysiology of their disease [3,4]. The Amer-
ican Thoracic Society has defined dyspnea in the following way: ‘‘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, psy-
chological, social and environmental factors, and may induce secondary
physiological and behavioral responses’’ [5]. For the purpose of this article,
the authors use the terms ‘‘dyspnea’’, ‘‘breathlessness,’’ and ‘‘shortness of
breath’’ interchangeably.

* Corresponding author.
E-mail address: pamelung@umaryland.edu (P.J. Amelung).

0095-4543/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved.
doi:10.1016/j.pop.2006.06.007 primarycare.theclinics.com
644 SARKAR & AMELUNG

Prevalence of dyspnea
Breathing discomfort is a common symptom experienced by patients, and
can be quite distressing. It has more than 30 attributed causes involving mul-
tiple organ systems [6]. There are no precise data on the prevalence of dysp-
nea. The actual scope of the problem varies among clinical settings and
patient subgroups. Population-based surveys have estimated the prevalence
to be between 17% and 38% [7–9]. In an ambulatory setting the prevalence
of dyspnea was 3.7% [10]. Morbidity associated with dyspnea can range
from minor to disabling. Dyspnea is often associated with cardiac and respi-
ratory diseases, but it can also be caused by obesity and deconditioning. As
these conditions increase, the population with the complaint of dyspnea will
rise too.

Mechanisms of dyspnea
The difficulty in determining the cause of shortness of breath results from
the complex and poorly understood pathophysiology involved in the
production of the sensation of breathlessness. The mechanism of dyspnea
originates with the activation of sensory systems involved with respiration.
One or more receptors can be individually or collectively stimulated to
initiate an afferent signal to the central nervous system (CNS). This afferent
impulse is then transmitted to the central nervous system. Here the message
is processed and efferent impulse is directed to the respiratory system.
The major receptor sites considered in the sensation of dyspnea include
chemoreceptors, mechanoreceptors, and lung receptors. Chemoreceptors
are located both centrally (medulla) and peripherally (carotid and aortic
bodies), and are responsible for detection of changes in oxygen and carbon
dioxide. Stimulation of these receptors causes changes that adjust breathing
to maintain blood gas and acid-base homeostasis. An increase in carbon di-
oxide stimulates central receptors and results in an increase in ventilation.
Hypoxia stimulates respiration through its effects on the peripheral chemo-
receptors, which may cause breathlessness in patients who have underlying
lung disease. It has also been observed that supplemental oxygen adminis-
tration relieves dyspnea in some patients who have lung disease, even in
the absence of any changes in ventilation. Various mechanoreceptors, in-
cluding chest wall receptors, may also be important in the generation of
the sensation of dyspnea [11]. Upper airway receptors can modify the sensa-
tion of dyspnea, based on clinical observations that patients sometimes re-
port a decrease in the intensity of their shortness of breath when sitting
by a fan or open window. Afferent information from pulmonary vagal re-
ceptors project to the CNS and are important in shaping the pattern of
breathing and to the sensation of dyspnea [12,13]. These impulses, with af-
ferent impulses generated from various receptors, are received and processed
in the CNS. The motor cortex or brainstem respiratory neurons are thought
 EVALUATION OF THE DYSPNEIC PATIENT IN THE OFFICE 645

to transmit a signal to the sensory cortex, which might contribute to a ‘‘sense

of effort’’ to breathing [14,15]. This sensation increases whenever the central
motor command is increased or whenever the respiratory muscles become
weak or fatigued. Based on response to the afferent information, the CNS
sends an efferent impulse via the phrenic nerve to the diaphragm and other
respiratory muscles to increase respiration. It is not completely understood
how this impulse affects different aspects of breathing. In 1963 the concept
of ‘‘length-tension inappropriateness’’ was proposed by Campbell and Ho-
well [16]. According to their theory, there was a disassociation between the
force or tension generated by the respiratory muscles and the lung volume
generated by that force. Currently, mismatch between afferent information
to the CNS and outgoing motor command is thought to lead to the sensa-
tion of breathlessness. The afferent feedback from peripheral sensory recep-
tors may allow the brain to assess the effectiveness of the motor commands
issued to the ventilatory muscles; that is, the appropriateness of the response
in terms of flow and volume for the command. When changes in respiratory
pressure, airflow, or movement of the lungs and chest wall are not appropri-
ate for the outgoing motor command, the intensity of dyspnea is heightened.
In other words, dissociation between the motor command and the mechan-
ical response of the respiratory system may produce a sensation of respira-
tory discomfort. Today the theory has been generalized to include not only
information arising in the ventilatory muscles, but information emanating
from receptors throughout the respiratory system, and has been termed
‘‘neuromechanical dissociation’’ [14,17].

Approach to patients who have dyspnea

In the outpatient setting, dyspnea is a common symptom. Establishing
a cause can at times be difficult, because dyspnea is a symptom of a myriad
of disorders, ranging from the completely benign to the relatively serious;
however, asthma, congestive heart failure (CHF), chronic obstructive pul-
monary disease (COPD), pneumonia, cardiac ischemia, psychogenic, and in-
terstitial lung disease have been found in some series to account for
approximately 85% of all cases of shortness of breath [18–22]. For a dys-
pneic patient presenting to the office, the initial goal is to determine the se-
verity of the dyspnea and the need for urgent intervention such as
intubation. The clinical approach to the patient depends on the acuteness
of the problem. Although most patients who are unstable usually present
to local hospitals, primary care physicians must be prepared and equipped
to triage, manage, and stabilize patients who have acute dyspnea.

Evaluation of acute dyspnea

For acute shortness of breath, an initial quick evaluation should consist
of assessment of airway patency and auscultation of the lungs. The
646 SARKAR & AMELUNG

breathing pattern and rate should be determined and use of accessory mus-
cles noted. Cardiac rhythm, vital signs, and pulse oximetry should be mon-
itored. The mental status should be evaluated, and a brief history of cardiac
and pulmonary disease obtained if not already known. Unstable patients
typically have hypotension, hypoxemia, tracheal deviation, altered mental
status, unstable arrhythmia, stridor, retractions, cyanosis, or absent breath
sounds signaling the acuity of their problem. These patients should be ad-
ministered oxygen, have intravenous (IV) access established, and be given
initial treatment as appropriate (bronchodilators, diuretics). Consideration
should be given to needle decompression if the initial diagnostic impression
is pneumothorax, and to intubation if necessary. Unstable patients should
be transported to the closest emergency department for further evaluation
and treatment. Trained health care personnel should accompany the patient
and continue management until supervision is transferred to the emergency
department team.
For acute problems, the differential diagnosis is relatively narrow; they
are in general related to disease of the respiratory or cardiac systems. The
differential diagnosis of these two systems will cover the most common dis-
eases encountered with acute shortness of breath: COPD, asthma, pneumo-
nia, pulmonary embolism, pneumothorax, heart failure, and myocardial
infarction. There are many other physical causes of acute shortness of
breath, however, including acute renal failure, diabetic ketoacidosis, septice-
mia, or other metabolic acidoses with respiratory compensation. Acute
dyspnea may also be psychogenic in origin, although this should be a diag-
nosis of exclusion (Table 1).
Once an emergent situation has been excluded, the assessment of the sta-
ble patient who complains of acute shortness of breath includes a medical
history, physical examination, and appropriate laboratory testing. A com-
prehensive patient history is the starting point for evaluating dyspnea. It
is imperative to characterize the dyspnea in terms of descriptive qualities,
onset, frequency, intensity, duration, triggers (exposures), provoking activi-
ties (ambulation, eating, changing position), associated respiratory symp-
toms, and strategies or actions (medications, positions) that provide relief.
Intermittent dyspnea may be caused by asthma or heart failure, whereas per-
sistent or progressive dyspnea suggests other chronic conditions, such as
COPD, interstitial fibrosis, or pulmonary hypertension. Nocturnal dyspnea
is may be indicative of asthma, CHF, or gastroesophageal reflux. Dyspnea
occurring independent of physical activity suggests possible psychological
etiology, or possibly allergic or mechanical problems. Dyspnea occurring
mainly after exercise suggests exercise-induced asthma.
A complete history should emphasize any coexisting cardiac and pulmo-
nary symptoms. For example, the presence of cough may imply asthma or
pneumonia; cough combined with a change in character of sputum may
be caused by exacerbation of COPD. The symptoms of fever, sore throat,
and acute dyspnea may suggest epiglottitis. Chest pain during dyspnea
 EVALUATION OF THE DYSPNEIC PATIENT IN THE OFFICE 647

Table 1
Acute dyspnea: etiologies and characteristics
Physical
Disorder History findings examination Chest radiograph
Cardiac: CHF, Chest pain, Cyanosis, crackles, Cardiomegaly,
ACS, orthopnea, edema, JVD, pleural effusion,
arrhythmia, PND, edema, murmurs, S3 or interstial edema
anemia palpitations S4, HJR,
pericarditis hypertension
COPD Worsening Pursed-lip Hyperinflated
exacerbation dyspnea, breathing, lungs
increased wheezing, barrel
sputum volume, chest, decreased
increased breath sounds,
sputum prolonged
purulence expiratory phase
Asthma History of asthma, Wheezing, cough, Hyperinflated
exacerbation allergy history, tachycardia, lungs
increased prolonged
reliance on expiratory phase
beta-agonists,
chest tightness
Pneumonia Fever, cough, Fever, crackles, Parenchymal
purulent sputum decreased breath infiltrate
sounds,
increased
fremitus
Pulmonary Pleuritic chest Wheezing, friction Normal,
embolism pain, lower rub, lower atelectasis,
extremity extremity effusion,
pain/swelling, swelling wedge-shape
predisposing risk density
factors
Pneumothorax Pleuritic chest pain Unilateral Air in pleural space
hyperresonance, with collapsed
absent breath lung, shift of
sounds, tracheal mediastium
shift
Upper airway History of Stridor, wheezing Visualized foreign
obstruction: choking, body, air
laryngospasm, gurgling trapping,
aspirated foreign respirations, hyperinflation
body persistent
pneumonias
Psychogenic: Emotional upset, Sighing Normal
hyperventilation, feeling
anxiety, panic impending
attacks doom, neurotic
personality
Abbreviations: ACS, acute coronary syndrome; CHF, congestive heart failure; HJR, hepa-
tojugular reflux; JVD, jugular venous dyspnea; PND, paroxysmal nocturnal dyspnea.
648 SARKAR & AMELUNG

may be caused by coronary or pleural disease, depending on the quality and

description of the pain. Pleuritic chest pain could be caused by pneumotho-
rax, pulmonary embolism, pneumonia, or pleuritis. Palla and colleagues [23]
found that dyspnea or tachypnea with pleuritic chest pain occurred in 97%
of patients who had clinically significant pulmonary embolism. Anginal
chest pain accompanied by shortness of breath may signify ischemia associ-
ated with left ventricular dysfunction. Lusiani and coworkers [24] found that
parxosymal dyspnea or pulmonary edema may be the only clinical presenta-
tion in 10% of patients who have myocardial infarction. Based on this infor-
mation, along with the physical examination, the physician should be able to
categorize the cause of the acute dyspnea as either suspected pulmonary,
suspected cardiac, or other. Although cardiopulmonary disease may be
most likely, it is important that consideration of causes of acute dyspnea
other than cardiopulmonary be kept in mind. Inquire about indigestion or
dysphagia, which may indicate gastroespophageal reflux with aspiration.
Anxiety symptoms may imply psychogenic causes of dyspnea, but organic
etiologies always should be excluded. For example, Saisch and colleagues
[25] found that the most common complaint in patients diagnosed with
acute hyperventilation syndrome was dyspnea. Additional information
about social history (cigarette smoking, occupation, current or previous in-
halational exposures, hobbies, and so forth) is essential. Table 1 summarizes
clues in the history that help in the diagnosis in dyspnea.
The physical examination should include the neck, thorax, lungs, heart,
and extremities. Selected abnormal findings on the physical examination
and clinical relevance are shown in Table 1. The general appearance and vi-
tal signs can be used to determine the severity of dyspnea by observing re-
spiratory effort, use of accessory muscles, mental status, and ability to
speak. The neck area might reveal a shift of the trachea, jugular venous dis-
tention, an enlarged thyroid gland, or adenopathy. Auscultate for stridor,
because it may be indicative of an upper airway obstruction. Inspection of
thorax might show an increased anterior-posterior diameter or chest wall
deformity. Palpate the chest for subcutaneous emphysema and crepitus,
and percuss for dullness, an indication of consolidation or effusions. On
the other hand, hyperresonance on percussion suggests pneumothorax or
bullous emphysema. Auscultation of breath sounds should focus on inten-
sity, timing of the respiratory phases, and any adventitial sounds. Absent
breath sounds may be consistent with pneumothorax or pleural effusion.
Wheezing indicates turbulent airflow, which can be caused by asthma,
COPD, and left ventricular failure. Key features of the heart examination
include point of maximal impulse, the presence of any heart murmur, and
a possible gallop. Rapid or irregular pulse may signify a dysarrhythmia.
An S3 gallop suggests a left ventricular dysfunction in congestive heart fail-
ure. A loud P2 may be heard in patients who have pulmonary hypertension
and cor pulmonale. Check the lower extremities for cyanosis or clubbing.
Digital clubbing can be notable for cancer or a chronic respiratory condition
 EVALUATION OF THE DYSPNEIC PATIENT IN THE OFFICE 649

other than COPD. Edema of lower extremities suggests congestive failure if

symmetric and thromboembolic disease if asymmetric.
Using information obtained from the medical history and physical exam-
ination, the physician should be able to form a working hypothesis as to the
most likely cause of the dyspnea. Developing a differential diagnosis is impor-
tant to focus further diagnostic testing. This is preferable to ordering a battery
of tests at the initial evaluation. The office work-up depends on the modalities
available. The initial diagnostic work-up usually includes a chest radiograph,
a resting electrocardiogram, and a complete blood count. On the other hand,
if a diagnosis of asthma or COPD is initially suspected, then pulmonary func-
tion testing (PFT) and pulse oximetry are important first steps. The preva-
lence of positive chest radiographic findings in patients who present to
acute care clinics with complaints of chest-related symptoms has been shown
to be 34.8% for all ages and up to 47% for patients over the age of 40 years
[26]. Although the chest radiograph is usually not diagnostic, it can provide
useful information about cardiac size and configuration, lung parenchyma,
pulmonary vasculature, the pleural space, mediastinum, and position of the
diaphragm. The 12-lead resting electrocardiogram rarely establishes an initial
diagnosis, but it does provide important data about ischemia, arrhythmias,
and chamber size. The complete blood count screens for anemia, which can
effect the oxygen carrying capacity and exert a physiologic stress that may
contribute to dyspnea. On the other hand, polycythemia may be the only
clue to hypoxia, and indicates a more chronic, rather than acute, process.
Additional testing depends on whether a primary pulmonary or cardiac
disease is considered as the most likely cause for breathlessness. Left heart
failure owing to ischemia or cardiomyopathy, pericardial effusion, and val-
vular dysfunction can all lead to dyspnea. Although the history, physical ex-
amination, and basic laboratory tests may be helpful to evaluate these
conditions, sending the patient for an echocardiogram will provide ex-
tremely useful information about chamber size, ventricular function, valvu-
lar function, possible pericardial effusion, and an estimate of pulmonary
artery systolic pressure. Studies have shown several potential mechanisms
for dyspnea in patients who have cardiac disease: an elevated pulmonary ve-
nous pressure, respiratory muscle weakness, bronchial hyperresponsiveness,
and an augmented ventilatory response to exercise associated with an in-
creased dead space to tidal volume ratio [27–30]. Concomitant obstructive
airway or restrictive disease may also be present in patients who have car-
diac disease. For example, Myers and Froelicher [29] looked at exercise he-
modynamic determinants of exercise capacity in patients who have heart
failure, and found that relative hyperventilation is commonly observed dur-
ing exercise in patients who have heart failure, and is related to ventilation-
perfusion mismatching in the lung caused by a higher-than-normal fraction
of physiologic dead space [29]. Also, Snashall and Chung [30] described how
airway narrowing may be precipitated by acute elevation of pulmonary or
bronchial vascular pressures. This appears to be mainly caused by reflex
650 SARKAR & AMELUNG

bronchoconstriction, and can occur in left ventricular failure, mitral steno-

sis, and pulmonary edema. Therefore selected pulmonary function tests may
also be indicated to evaluate dyspnea in patients who have suspected cardiac
disease.
Establishing heart failure as a cause of dyspnea in patients presenting to
primary care clinics is not always possible based on symptoms and physical
findings, and patients may need to be sent for laboratory testing. With heart
failure ventricular cells are recruited to secrete both atrial natriuretic peptide
and brain natriuretic peptide (BNP). These markers are secreted from both
the left and the right cardiac ventricle in response to ventricular volume ex-
pansion and pressure overload. Recent studies have suggested that these
neurohormones are reliably elevated in the setting of congestive heart failure
and may be very helpful in its diagnosis [31–33]. The use of rapid BNP test-
ing in addition to clinical judgment increased the accuracy of the clinical
evaluation. McCullough and colleagues [34] evaluated the value of rapid
measurement of plasma BNP for distinguishing between heart failure and
a pulmonary cause of dyspnea in approximately 1600 patients presenting
with a major complaint of acute dyspnea. The final diagnosis was heart fail-
ure in 47%, no heart failure in 49%, and noncardiac dyspnea in patients
who had a past history of left ventricular dysfunction in 5%. The study dem-
onstrated that plasma concentrations of BNP were markedly higher in pa-
tients who had clinically diagnosed heart failure (both left and right)
compared with those who did not have heart failure (mean of 675 versus
110 pg/ml). Intermediate values were found in the patients who had baseline
left ventricular dysfunction but not acute exacerbation (346 pg/ml). A value
greater than 100 pg/ml diagnosed heart failure with a sensitivity, specificity,
and predictive accuracy of 90%, 76%, and 83%, respectively. The predictive
accuracy of plasma BNP for heart failure was equivalent to or better than
other parameters such as cardiomegaly on chest radiograph, a history of
heart failure, or rales on physical examination [34]. Currently, with the rapid
assay most dyspneic patients who have heart failure have values above
400 pg/ml, whereas values below 100 pg/ml have a very high negative
predictive value for heart failure as a cause of dyspnea.
A pulmonary function test is the starting point for evaluation of sus-
pected respiratory disease. In the acute setting, simple office spirometry
may be the only test easily available. The presence of acute airways obstruc-
tion will be suggested by the finding of reduced forced expiratory volume in
one second (FEV1) and reduced FEV1 to forced vital capacity (FVC) ratio.
This will typically indicate acute asthma or an exacerbation of COPD. As an
alternative to spirometry, peak expiratory flow rates (PEFR) can be mea-
sured with a simple handheld device. These measurements are especially use-
ful in acutely dyspneic patients who have known baseline measurements so
that comparisons can be made. The flow-volume loop is most useful in the
evaluation of upper-airway obstruction. Although an abnormal flow-vol-
ume loop may not be diagnostic, it can provide clues to specific diagnoses
 EVALUATION OF THE DYSPNEIC PATIENT IN THE OFFICE 651

such as obstruction, restriction, or intrathoracic/extrathoracic airways ob-

struction. The utility of measuring D-dimer as a noninvasive method to di-
agnosis deep venous thromboembolism and pulmonary embolism has been
studied extensively. D-dimer is a specific degradation product released into
the circulation when cross-linked fibrin undergoes endogenous fibrinolysis.
Perrier and colleagues [35] have shown that a D-dimer level measured by
an enzyme-linked immunosorbent assay of less than 500 ng/ml has a negative
predictive value of greater than 95% of excluding a pulmonary embolism in
a patient who has low pretest clinical probability. A negative quantitative
rapid enzyme-linked immunosorbent assay (ELISA) result is as diagnosti-
cally useful as a normal lung scan or negative duplex ultrasonograpy finding
for excluding venous thromboembolism (VTE). The D-dimer is unidirec-
tional in that a negative test is useful in ruling out pulmonary embolism,
but a positive test does not have a sufficiently high specificity or positive like-
lihood ratio to be helpful in increasing the certainty of a diagnosis of pulmo-
nary embolism. D-dimer results are unlikely to be helpful in patients who
have had recent surgery (within 3 months) or who have malignancy, because
these patients often have values above 500 ng/ml [36].

Evaluation of chronic dyspnea

The patient who has chronic shortness of breath may be more difficult to
diagnose because the dyspnea typically develops over weeks to months, pa-
tients alter their activities in response to the dyspnea so the severity may not
apparent, and dyspnea is frequently out of proportion to any physiologic
impairment that is found. In spite of this difficulty, however, the majority
of patients who have chronic shortness of breath will have either asthma,
COPD, interstitial lung disease, or cardiomyopathy [21].
The history is important in chronic dyspnea, but should be considered
only part of the systematic evaluation that is necessary; the initial physician
impression of the etiology of dyspnea based on the history alone was correct
only 66% of the time in one study [21]. Patients may have difficulty describ-
ing the exact sensation of their dyspnea. They should be questioned about
the onset, frequency and duration of breathlessness, as well as triggers
and strategies that provide relief. Intermittent dyspnea is more likely caused
by reversible events, such as bronchoconstriction, pleural effusion, CHF, or
even chronic recurrent thromboemboli. Progressive dyspnea more likely
stems from COPD, neuromuscular disorders, or interstitial lung disease. As-
sociated symptoms should be sought, including cough, sputum, wheezing,
orthopnea, chest pain, heartburn, and paroxysmal nocturnal dyspnea. In
general, the sensation of increased work or effort of breathing is common
to most dyspneic patients; however, if asked to choose from a list of descrip-
tors, the sensation that most accurately describes their dyspnea, patients
who have different diseases will choose different groups of descriptors
[37,38].
652 SARKAR & AMELUNG

Physical examination should focus on the neck, chest, lungs, heart, and
extremities. Obvious findings such as rales in CHF or distant breath sounds
in COPD and pleural effusion should be noted, but also note if deep inspi-
rations cause cough, which may indicate asthma or interstitial lung disease.
Wheezing may only become apparent after the patient is asked to forcefully
exhale. Careful evaluation of the heart sounds is needed to detect pulmonary
hypertension, and clubbing should not be overlooked. Table 2 outlines the
history and physical findings in chronic dyspnea.
Testing in chronic dyspnea should be targeted in attempt to answer spe-
cific questions. For example, if asthma or COPD is suspected, spirometry
should be ordered; a reduced FEV1 and FEV1/FVC ratio indicates obstruc-
tive airway disease. Bronchoprovocation can diagnose reactive airways

Table 2
Chronic dyspnea: etiologies and characteristics
Physical
Disorder History findings examination Chest radiograph
Right and left Chest pain, Cyanosis, crackles, Cardiomegaly,
heart failure orthopnea, edema, JVD, pleural effusion,
(CHF) PND, edema murmurs, S3 or interstial edema
S4, HJR,
hypertension
COPD Tobacco use, Pursed lip Hyperinflated
chronic cough breathing, lungs
wheezing, barrel
chest, decreased
breath sounds
Asthma Childhood history, Wheezing, cough Hyperinflated
allergy history lungs
ILD Gradual onset of Fine inspiratory Decreased lung
dyspnea, crackles volumes,
occupational & increased
environmental interstial
exposure markings,
fibrosis
Malignancy Cough, Decreased breath Mass, hilar
hemoptysis, sounds, clubbing adenopathy
shortness of
breath, fatigue,
fevers, night
sweats, weight
loss
Psychogenic: Emotional upset, Sighing Normal
hyperventilation, feeling
anxiety, panic impending
attacks doom, neurotic
personality
Anemia Fatigue, dyspnea Tachycardia, pale Normal
with exertion conjunctiva
Abbreviation: ILD, interstitial lung disease.
 EVALUATION OF THE DYSPNEIC PATIENT IN THE OFFICE 653

disease caused by asthma if spirometric values are normal. Flow volume

loops obtained during spirometry can suggest upper airway obstruction. Re-
strictive lung disease can be suggested by spirometric results (reduced FVC
and normal or increased ratio of FEV1/FVC ratio), but the measurement of
lung volumes is necessary to confirm restriction (reduced FVC and total
lung capacity). A reduced diffusing capacity, (DLco) is usually a sensitive
indicator of an abnormality in pulmonary gas exchange. It may be helpful
to identify patients who have emphysema (ie, a reduced DLco in the presence
of obstructive airway disease). In a patient who has normal spiromety and
lung volumes but a reduced DLco, the differential diagnosis could include
anemia, early interstitial lung disease and pulmonary vascular disease. The
measurement of inspiratory (PImax) and expiratory (PEmax) mouth
pressures is important in the evaluation of neuromuscular causes of dyspnea.
Cardiac etiologies of dyspnea include left heart failure, ischemia, pericar-
dial effusion, and valvular disease. As for acute dyspnea, an echocardiogram
can be extremely useful in the evaluation of chronic dyspnea, and provides
useful information about chamber size, valvular function, and cardiac func-
tion. An electrocardiogram (EKG) will reveal evidence of ischemia or ar-
rhythmia. An EKG done in conjunction with stress or exercise may
unmask a cardiac condition not evident at rest. Chest radiograph (CXR)
may show an enlarged heart, pulmonary vascular congestion, or vascular
pruning consistent with pulmonary hypertension.
If directed testing is not possible because the cause of dyspnea is unclear
from the history and physical examination, the basic work-up should in-
clude spirometry and diffusing capacity, a CXR, a resting 12-lead EKG,
and oximetry as initial screening tests. If the results of these tests are normal,
then anxiety/hyperventilation, deconditioning, and respiratory muscle
weakness are the likely etiologies. As previously suggested, PImax and
PEmax should be measured to evaluate respiratory muscle strength. Muscle
weakness can be isolated to the respiratory system or can be part of a systemic
process. For example, Flaherty and coworkers [39] described 28 patients
referred for unexplained breathlessness who had normal spirometry, lung
volumes, and gas exchange, but had reduced values for PImax and PEmax.
Based on muscle biopsies, it was confirmed that these patients were diagnosed
with mitochondrial myopathy, affecting their muscles of respiration.
If the source of dyspnea cannot be determined despite a complete pulmo-
nary and cardiac evaluation, cardiopulmonary exercise testing (CPET) can
be performed. The test will hopefully simulate the patient’s experience of
breathlessness and differentiate between pulmonary, cardiac, psychogenic,
and deconditioning as the source of the patient’s dyspnea. It can also be use-
ful if the severity of the patient’s dyspnea is greater than expected from the
results of objective measurements, or if the patient likely has both cardiac
and respiratory factors contributing to dyspnea. CPET stresses the oxygen
transport system, a complex network in which pathology at any point could
generate dyspnea. Measured responses to exercise are taken from various
654 SARKAR & AMELUNG

systems, so CPET can help identify whether the major abnormality lies in
the pulmonary or cardiac system. It can point to deconditioning, or periph-
eral vascular or muscular disease as potential contributors as well. Other less
commonly used tests in the work-up of chronic dyspnea include ventilation-
perfusion scanning (chronic thromboembolic disease), thyroid function tests
(occult hyper- or hypothyroidism) or gallium scanning (inflammatory lung
disease or infection).

Treatment of dyspnea
Treatment of the underlying disease is the most effective method of alle-
viating dyspnea: bronchodilators for acute or chronic dyspnea related to
asthma or COPD, diuretics for breathlessness caused by acute or CHF, ox-
ygen and antibiotics for shortness of breath related to pneumonia. If the
specific cause of the dyspnea is elusive, or if a specific treatment is not avail-
able, then treatment should be aimed at treating the symptom. Patients who
have chronic dyspnea can be taught a variety of methods to help them alle-
viate or cope with their breathlessness. Pursed-lips breathing can increase
the tidal volume, decrease the respiratory rate, and improve saturation in
patients who have COPD, thereby relieving their dyspnea [40]. Diaphrag-
matic breathing is another strategy to help reduce dyspnea. Patients can
be taught energy conservation techniques to both reduce their respiratory
effort and improve their respiratory muscle function. Pulmonary rehabilita-
tion, or physical training, has been shown to reduce dyspnea, based on abil-
ity to perform activities of daily living and perform exercise testing [41,42].
The physical training need not be extreme to afford benefit; even simple re-
sistance training with weights has been shown to improve muscle strength
and endurance [43,44]. Patients should understand that reaching goals
may take months of training, and therefore motivation and commitment
on their part is essential. Oxygen can be used to reduce respiratory drive,
thereby reducing dyspnea. Oxygen can improve respiratory muscle function
[45] and pulmonary artery pressure [46]. Oxygen is usually dosed to prevent
desaturation, but higher levels may improve exercise performance [47]. Psy-
chotropic medications, including anxiolytics and antidepressants, have not
proven to be of benefit in relieving dyspnea [48]; however, these may be con-
sidered in patients who exhibit these symptoms in relation to their dyspnea.
Although the role of opiates is well-accepted in relieving terminal dyspnea,
the benefits have been inconsistent and side effects frequent when studied in
long-term but nonterminal dyspneic patients [49].

Summary
Dyspnea is a nonspecific symptom of any disease involving the respira-
tory system. Although diseases of the lungs, chest wall, pleura, diaphragm,
 EVALUATION OF THE DYSPNEIC PATIENT IN THE OFFICE 655

upper airway, and heart are most common, diseases of many other organ
systems (eg, neuromuscular, skeletal, renal, endocrine, rheumatologic, he-
matologic, and psychiatric) may involve the respiratory system and present
with dyspnea. Dyspnea should be evaluated systematically, and a thorough
history and physical examination and baseline tests of heart and lung func-
tion are necessary to establish a complete database. More sophisticated test-
ing may be needed when the cause is not readily apparent from the initial
work-up. Treatment is best and most effective when geared toward a specific
etiology, but if this is not possible, nonspecific treatment of the symptom pf
dyspnea may afford the patient some benefit.

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