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Disnea - Evaluation of the adult with dyspnea in the emergency department - UpToDate 2013
 

Disnea - Evaluation of the adult with dyspnea in the emergency department - UpToDate 2013

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Evaluation of the adult with dyspnea in the emergency department - UpToDate 2013

Evaluation of the adult with dyspnea in the emergency department - UpToDate 2013

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    Disnea - Evaluation of the adult with dyspnea in the emergency department - UpToDate 2013 Disnea - Evaluation of the adult with dyspnea in the emergency department - UpToDate 2013 Document Transcript

    • Evaluation of the adult with dyspnea in the emergency department Authors Azeemuddin Ahmed, MD, MBA Mark A Graber, MD, FACEP Literature review current through: Jun 2013. | This topic last updated: ene 22, 2013. 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 "Hereditary angioedema: Treatment of acute attacks" 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 manifestations and diagnosis of Bordetella pertussis infections 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 "Initial evaluation and management of 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: 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 "Initial evaluation and management of 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 "Clinical manifestations, diagnosis, and evaluation 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 "Salicylate (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 "Evaluation and 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: Initial testing".)  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 "Evaluation of adults 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 "Initial evaluation and management of 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 "Salicylate (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 "Salicylate (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 acute decompensated heart failure (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. Note that measurements of the respiratory rate obtained during triage may not be accurate [20,21].  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 [22,23]. 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 [24]. (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 [25]. 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 [26]. 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 [27]. The length of stay of patients presenting to the ED with acute dyspnea may be slightly reduced if BNP testing is performed [28]. 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".) 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 blood gases" and"Venous blood gases and other alternatives to arterial blood gases".) 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 [29,30]. 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 [31]. 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 of adults 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 topic (see "Patient information: Shortness of breath (dyspnea) (The Basics)")  Beyond the Basics topic (see "Patient information: Shortness of breath (dyspnea) (Beyond the Basics)") 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, heart, 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.) Use of UpToDate is subject to the Subscription and License Agreement. REFERENCES 1. Simon PM, Schwartzstein RM, Weiss JW, et al. Distinguishable sensations of breathlessness induced in normal volunteers. Am Rev Respir Dis 1989; 140:1021. 2. American College of Emergency Physicians. www.acep.org/webportal/Newsroom/NewsMediaResources/StatisticsData/default.htm (Accessed on February 04, 2006). 3. Ray P, Birolleau S, Lefort Y, et al. Acute respiratory failure in the elderly: etiology, emergency diagnosis and prognosis. Crit Care 2006; 10:R82. 4. Herzon FS, Martin AD. Medical and surgical treatment of peritonsillar, retropharyngeal, and parapharyngeal abscesses. Curr Infect Dis Rep 2006; 8:196. 5. Saifeldeen K, Evans R. Ludwig's angina. Emerg Med J 2004; 21:242. 6. Sethi DS, Stanley RE. Deep neck abscesses--changing trends. J Laryngol Otol 1994; 108:138. 7. Berg S, Trollfors B, Nylén O, et al. Incidence, aetiology, and prognosis of acute epiglottitis in children and adults in Sweden. Scand J Infect Dis 1996; 28:261. 8. Newton E, Mandavia S. Surgical complications of selected gastrointestinal emergencies: pitfalls in management of the acute abdomen. Emerg Med Clin North Am 2003; 21:873. 9. Angueira CE, Kadakia SC. Effects of large-volume paracentesis on pulmonary function in patients with tense cirrhotic ascites. Hepatology 1994; 20:825. 10. Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med 2003; 65:963. 11. Simon PM, Schwartzstein RM, Weiss JW, et al. Distinguishable types of dyspnea in patients with shortness of breath. Am Rev Respir Dis 1990; 142:1009. 12. Bass C. Chest pain and breathlessness: relationship to psychiatric illness. Am J Med 1992; 92:12S. 13. Martinez FJ, Stanopoulos I, Acero R, et al. Graded comprehensive cardiopulmonary exercise testing in the evaluation of dyspnea unexplained by routine evaluation. Chest 1994; 105:168. 14. Retractions www.nlm.nih.gov/medlineplus/ency/article/003322.htm (Accessed on February 02, 2006). 15. Wipf JE, Lipsky BA, Hirschmann JV, et al. Diagnosing pneumonia by physical examination: relevant or relic? Arch Intern Med 1999; 159:1082. 16. Leuppi JD, Dieterle T, Koch G, et al. Diagnostic value of lung auscultation in an emergency room setting. Swiss Med Wkly 2005; 135:520. 17. Metlay JP, Kapoor WN, Fine MJ. Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination. JAMA 1997; 278:1440. 18. Chakko S, Woska D, Martinez H, et al. Clinical, radiographic, and hemodynamic correlations in chronic congestive heart failure: conflicting results may lead to inappropriate care. Am J Med 1991; 90:353. 19. Mueller C, Frana B, Rodriguez D, et al. Emergency diagnosis of congestive heart failure: impact of signs and symptoms. Can J Cardiol 2005; 21:921. 20. Lovett PB, Buchwald JM, Stürmann K, Bijur P. The vexatious vital: neither clinical measurements by nurses nor an electronic monitor provides accurate measurements of respiratory rate in triage. Ann Emerg Med 2005; 45:68.
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