Evaluation of the adult with dyspnea in the emergency department

Authors
Azeemuddin Ahmed, MD, MBA
Mark A Graber, MD, FACEP
Eric W Dickson, MD, MHCM, FACEP
Section Editor
Robert S Hockberger, MD, FACEP
Deputy Editor
Jonathan Grayzel, MD, FAAEM

Disclosures
Last literature review version 19.3: Fri Sep 30 00:00:00 GMT 2011 | This topic last
updated: Tue Sep 20 00:00:00 GMT 2011 (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
angioedema" and "An overview of angioedema: Pathogenesis and causes".)
 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, oral contraceptive use and smoking, and a personal or family history
 of hypercoagulability. Presentation varies widely, but dyspnea at rest and
tachypnea are the most common signs. A large minority of patients have no
known risk factor at the time of diagnosis. Other embolic phenomena 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 life-threatening 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 erythematosus). (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
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".)
 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 sufficiently
severe injury or one affecting regions involved in respiration. Such abnormalities
may 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-Barré syndrome, myasthenia gravis, and amyotrophic lateral
sclerosis, can cause weakness of the respiratory muscles, leading to acute
respiratory failure. (See "Epidemiology and clinical features of multiple sclerosis in
adults" and "Clinical features and diagnosis of Guillain-Barré syndrome in
adults" and "Clinical manifestations of myasthenia gravis" and "Clinical features of
amyotrophic lateral sclerosis and other forms of motor neuron disease".)

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 "Massive hemoptysis: Initial management".)
 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 breathe 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 [15-
19].
 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 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.
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 (lobar versus diffuse
disease) does not accurately predict the nature of the pneumonia (typical versus
atypical). (See "Diagnostic approach to community-acquired 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 (hypotension, elevated neck veins, unilateral diminished or absent
breath sounds) 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 changes

constitutes strong evidence supporting the diagnosis of cardiac ischemia. However,
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 effusion (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 (eg, troponin I) 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]. The length of stay of patients presenting to the ED with acute dyspnea
may be slightly reduced if BNP testing is performed [26].
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 "Natriuretic
peptide measurement in heart failure and other 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, PERC rule) 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 and venous 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".)

A venous blood gas 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. A normal or elevated CO2 in the
setting of dyspnea and tachypnea portends respiratory failure.

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 who have a normal chest radiograph.

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 [27,28]. 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-Barré) 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 [29]. 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 cricothyrotomy
(cricothyroidotomy)".)

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 two or three 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. However, failure to oxygenate the patient may have
profoundly adverse consequences. 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: General considerations".)

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 ventilation-perfusion (V/Q) mismatch, while rapid
improvement following treatment with bronchodilators strongly suggests
bronchoconstriction. Failure to improve with oxygen administration may indicate a right
to left shunt. (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 when appropriate. 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.
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education
materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are
written in plain language, at the 5th to 6th grade reading level, and they answer the four
or five key questions a patient might have about a given condition. These articles are
best for patients who want a general overview and who prefer short, easy-to-read
materials. Beyond the Basics patient education pieces are longer, more sophisticated,
and more detailed. These articles are written at the 10th to 12th grade reading level and
are best for patients who want in-depth information and are comfortable with some
medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you
to print or e-mail these topics to your patients. (You can also locate patient education
articles on a variety of subjects by searching on “patient info” and the keyword(s) of
interest.)

 Basics topics (see "Patient information: Shortness of breath (dyspnea) (The

Basics)")
 Beyond the Basics topics (see "Patient information: Shortness of breath
(dyspnea)")

SUMMARY AND RECOMMENDATIONS

 Dyspnea is the perception of an inability to breathe comfortably and is a common

chief complaint among emergency department patients. The differential diagnosis
of dyspnea is broad and may involve abnormalities affecting the upper airway,
lungs, chest wall, diaphragm, and nervous system, including both mechanical and
chemical receptors. The differential diagnosis is described by organ system in the
text (table 1). (See 'Differential diagnosis' above.)
 Common life-threatening causes of acute severe dyspnea 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)

 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. (See 'Epidemiology' above.)
 Important elements of the history and physical examination in patients with acute
dyspnea are described in the text. (See 'History' above and 'Physical
examination' above.)
 Signs that portend imminent respiratory arrest include:

 Depressed mental status

 Inability to maintain respiratory effort
 Cyanosis

 Many patients in respiratory distress often appear anxious and sit bolt upright or
in a tripod position. They often breathe rapidly. 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

 A plain chest radiograph and an electrocardiogram are obtained in most

emergency department (ED) patients with acute dyspnea. Dyspnea biomarker
panels do not appear to improve accuracy beyond clinical assessment and
focused testing. The use of ancillary studies in the patient with acute dyspnea is
discussed in the text. (See 'Ancillary studies' above.)
 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; and, establish the most likely
causes of dyspnea and initiate treatment. 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 'Initial interventions
and differential diagnosis' above and 'Emergent management' above.)