on 15-Mar-2021 (Mon)

Suspected interstitial lung disease is evaluated by HRCT, and central masses and suspected large airway obstruction (eg, tumor) are best evaluated by CT with contrast and direct visualization. On the other hand, vascular redistribution and abnormal heart size are best evaluated by measurement of a serum N-terminal pro-brain natriuretic peptide (NT-pro BNP) or transthoracic echocardiography.

A small percentage of patients with interstitial lung disease may have a normal chest radiograph on presentation; HRCT scan clearly is more sensitive for detecting subtle ground glass or reticular opacities [45,46]. Thus, patients with crackles on physical examination, reduced lung volumes on pulmonary function testing, or a decreased DLCO should have HRCT scans even if the chest radiograph is normal

If LV ejection fraction and end-diastolic volume are normal, echocardiography can identify features of diastolic dysfunction (heart failure with preserved ejection fraction [HF-PEF]), such as LV hypertrophy (LVH), concentric remodeling, and left atrial enlargement.

Among older adults with unexplained chronic dyspnea after an initial evaluation (eg, history, physical examination, pulmonary function tests, and a chest radiograph), nearly two-thirds have evidence of diastolic dysfunction [48], which can manifest as dyspnea with relatively minimal exertion.

Constrictive pericarditis can be difficult to diagnose in patients who present with chronic dyspnea, although patients generally have peripheral edema. Findings on echocardiography that may suggest constrictive pericarditis include increased pericardial thickness, dilation of the inferior vena cava with absent or diminished inspiratory collapse, abnormal filling of the ventricles in diastole, and pronounced respiratory variation in ventricular filling. When occult constrictive pericarditis is suspected, right heart catheterization is performed with measurement of hemodynamics before and after infusion of a liter of warm saline

When elevated pulmonary artery pressures are suggested by Doppler echocardiography and are supported by an elevated brain natriuretic peptide (BNP) and oxygen desaturation on exertion, the next step in the evaluation of suspected pulmonary hypertension is pulmonary artery catheterization to confirm an elevated mean pulmonary artery pressure (mPAP >20 mmHg at rest) and exclude diastolic dysfunction (unlikely with pulmonary artery wedge pressure [PAWP] <15 mmHg)

In particular, CPET may help identify patients with mitochondrial disorders (eg, McArdle’s myophosphorylase deficiency, isolated mitochondrial myopathy) by demonstrating a reduction in maximum oxygen uptake (VO₂ max), reduced peripheral oxygen extraction (increased mixed venous oxygen), and an increase in blood lactate after exercise.

A CPET may be helpful in providing support for the presence of deconditioning or in detecting a low threshold for respiratory discomfort. Patients with a low threshold for respiratory discomfort typically terminate the test at mild workloads because of dyspnea, but have no evidence of cardiopulmonary abnormality.

For patients who report dyspnea but have normal or near normal testing, we explain the reassuring nature of testing in detail, advise a conditioning program, and ask the patient to return in 6 to 12 months for re-evaluation.

For a given physiologic derangement that may cause dyspnea, perceptual responses vary widely among individuals. Anxiety, anger, pain, and depression may be associated with dyspnea intensity out of proportion to the physiologic impairment [55-58]. Increased ventilation associated with anxiety, anger, or pain may push an individual with a limited pulmonary reserve at baseline closer to his or her ventilatory limits and increase the perceived respiratory discomfort for any given activity.

Patients with hyperventilation syndrome typically experience a sensation of air hunger or an inability to take a deep breath in the absence of cardiopulmonary disease. These individuals may have panic and/or anxiety disorders, and on examination are often observed to breathe with very large tidal volumes despite the complaint that they cannot take a deep enough breath. (See "Hyperventilation syndrome in adults".)

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.

A chief complaint of dyspnea or shortness of breath accounts for 3.4 million visits (2.4 percent) of the more than 145 million visits to United States EDs in 2016. Other dyspnea-related chief complaints (eg, cough, chest discomfort) comprised 8.8 percent [2]

Epidemiologically, the most common diagnoses among older adult patients presenting to an ED with a complaint of acute shortness of breath and manifesting signs of respiratory distress (eg, respiratory rate >25, oxygen saturation [SpO2] <93 percent) are decompensated heart failure, pneumonia, chronic obstructive pulmonary disease (COPD), pulmonary embolism (PE), and asthma [4]

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 but is more common in children

Angioedema can cause significant swelling of the lips, tongue, posterior pharynx, and most dangerously the larynx; this can occur over minutes to hours and may cause severe dyspnea. The affected 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. Etiologies include idiopathic, allergic, medication-related (eg, nonsteroidal antiinflammatory drug [NSAID], angiotensin-converting enzyme [ACE] inhibitor, angiotensin receptor blocker), and complement-related (eg, C1-esterase inhibitor deficiency or a nonfunctional allele). Patients who receive intravenous (IV) tissue plasminogen activator (tPA) for acute ischemic stroke are also at risk for developing angioedema, which tends to be hemilingual and contralateral to the ischemic hemisphere [5].

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, and diarrhea).

Infections of the pharynx and neck – A number of oropharyngeal infections can cause acute dyspnea [6-9]. 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 in whom airway obstruction may not be a prominent symptom. 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.

Airway trauma – Blunt or penetrating injuries of the head or neck can cause hemorrhage, swelling, and anatomic distortion, 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 evaluated urgently. Early endotracheal intubation is often indicated.

Pulmonary embolism (PE) – The diagnosis of PE should be considered in any patient with acute dyspnea. Risk factors include a history of deep venous thrombosis or PE, prolonged immobilization, recent trauma or surgery (particularly orthopedic), pregnancy, malignancy, stroke or paresis, oral contraceptive or other estrogen use, 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 or associated with the acute chest syndrome of sickle cell disease; and amniotic fluid embolism.

Chronic obstructive pulmonary disease (COPD) – Exacerbations of 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

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. The chest may be silent in the face of severe bronchospasm. Extreme fatigue, cyanosis, and depressed mental status portend imminent respiratory arrest.

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, intubation, and barotrauma), a number of medical conditions increase the risk for developing a pneumothorax. (

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 "Pneumothorax in adults: Epidemiology and etiology".)

Patients with certain pulmonary diseases (including COPD, cystic fibrosis, tuberculosis, and AIDS patients with pneumocystis pneumonia) are at risk for secondary spontaneous pneumothorax. (See "Treatment of secondary spontaneous pneumothorax in adults".)

Patients who have sustained chest trauma or who have been coughing vigorously may develop a pneumothorax and 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 subacute unless underlying chronic pulmonary disease is present. A chest radiograph is generally necessary for diagnosis but may be unrevealing early in the disease course.

Noncardiogenic pulmonary edema (acute respiratory distress syndrome [ARDS]) – ARDS can complicate a wide range of conditions and is characterized by rapidly progressive dyspnea, hypoxia, and bilateral infiltrates on plain chest radiograph (CXR). It can be difficult to distinguish from acute decompensated heart failure purely on clinical grounds. Brain natriuretic peptide (BNP) and echocardiography can be helpful in differentiating the two. Even though a low BNP is helpful in differentiating ARDS from heart failure, an elevated BNP may occur with ARDS as well as with heart failure, and thus, clinical correlation is needed. Potential causes of ARDS include sepsis, shock, severe trauma, toxic inhalations (eg, aspiration, thermal injury, anhydrous ammonia, chlorine), infections (eg, hantavirus, severe acute respiratory syndrome [SARS], dengue, Middle East respiratory syndrome), blood transfusion, and drug overdose (eg, cocaine, opioids, aspirin).

High altitude pulmonary edema (HAPE) – HAPE is a form of noncardiogenic pulmonary edema that typically occurs in patients who have ascended rapidly to elevations over 2500 m (8000 feet). Symptoms often begin with a nonproductive cough, dyspnea on exertion, and fatigue, generally between two to four days after ascending to a high altitude. This may progress quickly to dyspnea at rest. Pulmonary symptoms are often accompanied by a headache and on occasion cerebral edema. The diagnosis of HAPE should be suspected in any patient with dyspnea who has ascended to a high altitude.

E-cigarette or vaping-associated lung injury (EVALI) – EVALI is an emerging cause of respiratory distress and lung injury, found especially among males (70 percent) less than 35 years of age (80 percent), although it can be seen in patients of any gender or age. It is primarily associated with vaping tetrahydrocannabinol (THC) products, but our understanding of this condition is evolving rapidly [10,11]. EVALI is characterized by a recent history of e-cigarette use; symptoms of shortness of breath, cough, chest pain, and gastrointestinal complaints; and diffuse hazy or consolidative opacities on plain radiograph.

Acute coronary syndrome (ACS) – Patients, particularly older adults, 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, rather than chest pain

Acute decompensated heart failure (ADHF) – Symptomatic ADHF can be caused by volume overload, heart failure with preserved ejection fraction (HFpEF [previously known as "diastolic dysfunction"]), heart failure with reduced ejection fraction (HFrEF [previously known as "systolic 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 emergency airway management. Common findings include tachypnea, pulmonary crackles, jugular venous distension (picture 1), S3 gallop, and peripheral edema. ADHF is among the most common causes of acute respiratory failure among patients over 65 years.

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. An elevated troponin may be seen secondary to demand ischemia.

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).

Cardiac arrhythmia – Cardiac rhythm abnormalities, such as atrial flutter, atrial fibrillation, second- and third-degree heart block, and tachyarrhythmias (eg, supraventricular tachycardia [SVT] and ventricular tachycardia) can result in dyspnea. Such abnormalities may stem from underlying disease, including myocardial ischemia or cardiac decompensation due to the elevated or slowed heart rate or uncoordinated contractions.

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.

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 (ECG) generally shows sinus tachycardia and low voltage and may uncommonly reveal electrical alternans.

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.

Neuromuscular disease – A number of neuromuscular diseases, including multiple sclerosis, Guillain-Barré syndrome, myasthenia gravis, amyotrophic lateral sclerosis, West Nile virus, and Enterovirus D68, seen primarily in children, can cause weakness of the respiratory muscles, leading to acute respiratory failure.