Approach to Adult Patients with Acute Dyspnea

      Keywords

      Key points

      • The cause of dyspnea is often evident from a complete history and physical examination.
      • Rapid determination of the cause of dyspnea saves lives.
      • Shortness of breath is not always primarily a pulmonary problem.
      • Understanding the pathophysiology of each disease allows clinicians to make rational decisions about testing.

      Introduction

      Emergency Medical Services (EMS) calls en route with a 45-year-old woman who has a history of congestive heart failure, chronic bronchitis, morbid obesity, and diabetes. She is breathing 40 times per minute, maintaining oxygen saturations of 94%. She appears mildly confused. You have 5 minutes to consider algorithms before the patient arrives. Perhaps respiratory therapy is paged to supply a ventilator or a biphasic positive airway pressure (BIPAP) machine. Maybe you prepare airway equipment or ask your nursing staff to access medication in advance, or you might use the time to expand your differential and determine what brief information regarding the patient’s history and initial physical examination will help you treat her.
      Acutely dyspneic patients present in various ways. Are the lungs full of fluid or pus? Did the throat swell shut or is the patient just anxious? Did the patient aspirate a foreign body or have a slow or rapid hemorrhage? Is the patient compensating for a severe metabolic acidosis or did the patient run out of beta agonists at home? This article provides helpful guidelines in the assessment and management of these diverse patients.
      Respiratory distress is responsible for nearly 4 million emergency department (ED) visits each year and is one of the most common presenting complaints in the elderly.
      • Prekker M.E.
      • Feemster L.C.
      • Hough C.L.
      • et al.
      The epidemiology and outcome of prehospital respiratory distress.
      When a patient presents with dyspnea, the primary task of the emergency physician is to assess for and ensure stability of the patient’s airway, breathing, and circulation. In the case of dyspnea, presentations may range from minor symptoms to extremis. Rapid assessment may necessitate the use of intubation, BIPAP, nebulizations, decompression, or other therapies in the immediate period following the patient’s arrival, to treat dyspnea.

      Patient evaluation

      The American Thoracic Society suggests that “dyspnea results from a … mismatch between central respiratory motor activity and incoming afferent information from receptors in the airways, lungs and chest wall structures.”
      • American Thoracic Society
      Dyspnea. Mechanisms, assessment, and management: a consensus statement.
      This dissociation can result from increased metabolic demand, decreased compliance, increased dead-space volume, or many other disorders that are discussed later. Each patient presenting short of breath uses a different set of phrases to describe the symptoms and examination reveals a different combination of disorders. The clinician’s ability to interpret these varying constellations is necessary to provide appropriate treatment to these patients, who are often in serious distress.

      History

      Acute dyspnea, or shortness of breath, is one of the most common chief complaints in the ED. The differential diagnosis includes many disorders that can be divided based on obstructive, parenchymal, cardiac, and compensatory features. A careful history can begin to narrow this wide differential. In addition to common symptoms, consider risk factors such as past medical and family history, trauma, travel, medications, and exposures.
      Schwartzstein and Lewis
      • Schwartzstein R.M.
      • Lewis A.
      Chapter 29: Dyspnea.
      use the analogy of a machine to identify different causes of dyspnea based on pathophysiologic data. Dysfunctions of the respiratory system may be caused by faulty controllers, ventilatory pumps, or gas exchangers (Table 1). This table makes it easier to understand the causes of shortness of breath related to respiratory causes.
      Table 1A systemic approach to dyspnea by assessing the components of the respiratory process
      Adapted from Schwartzstein RM, Lewis A. Dyspnea. In: Broaddus V, Mason RC, Ernst JD, et al, editors. Murray & Nadel's textbook of respiratory medicine. Elsevier health sciences. 6th edition. Philadelphia: Saunders/Elsevier; 2015.
      PartDescriptionManifestationsExamples
      ControllerMalfunction presents as abnormal respiratory rate or depth. Often related to abnormal feedback to brain from other parts of the systemAir hunger, need to breatheAbnormal feedback to brain from other systems. Metabolic acidosis, anxiety
      Ventilatory pumpComposed of muscles, nerves that signal the controller, chest wall, and pleura that create negative thoracic pressure, airways and alveoli allowing flow from atmosphere and gas exchangeIncreased work of breathing, low tidal volumesNeuromuscular problems (eg, Guillain-Barré), decreased chest wall compliance, pneumothorax, pneumonia, bronchospasm (COPD, asthma)
      Gas exchangerOxygen and carbon dioxide cross the pulmonary capillaries in the alveoli. Membrane destruction or interruption of the interface between the gas and capillaries by fluid or inflammatory cells limit gas exchangeIncreased respiratory drive, hypoxemia, chronic hypercapniaEmphysema, pneumonia, pulmonary edema, pleural effusion, hemothorax
      Cardiovascular disease manifests as dyspnea by causing disruptions of the system that pumps oxygenated blood to tissues and then transports the carbon dioxide back to the lung. Decreases in cardiac output or increases in resistance limit oxygen delivery. Similarly, decreased oxygen carrying capacity in anemia plays a role in its presentation with dyspnea.

      Physical Examination

      A detailed physical examination also provides important guidance (Table 2). Respiratory rate and oxygen saturation are obtained with vital signs. The clinician should assess the patient’s work of breathing, looking for any tripoding or retractions. Crepitance in the chest may indicate subcutaneous air and pneumothorax. Lung sounds such as wheezing, rales, and rhonchi further guide the differential. Decreased sounds, hyperresonance, or egophony may also provide additional clues.
      Table 2Physical examination findings and correlating diagnoses
      SymptomDifferential Diagnosis
      WheezeCOPD/emphysema, asthma, allergic reaction, CHF (cardiac wheeze)
      CoughPneumonia, asthma, COPD/emphysema
      Pleuritic chest painPneumonia, pulmonary embolism, pneumothorax, COPD, asthma
      OrthopneaAcute heart failure
      FeverPneumonia, bronchitis, TB, malignancy
      HemoptysisPneumonia, TB, pulmonary embolism, malignancy
      EdemaAcute heart failure, pulmonary embolism (unilateral)
      pulmonary edemaAcute and chronic heart failure, end stage renal and liver diseases, ARDS (sepsis)
      Tachypnea alonepulmonary embolism, acidosis (including aspirin toxicity), anxiety
      Abbreviations: ARDS, acute respiratory distress syndrome; CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; TB, tuberculosis.
      Jugular venous distension, S3 gallop, and peripheral edema indicate that a patient has fluid overload. Conjunctival pallor, capillary refill, and temperature of extremities can provide clues about blood volume and general circulation. Pulses must also be assessed.

      Testing

      Multiple tests are available to narrow the differential diagnosis of acute dyspnea. When using tests to augment clinical decision making, be sure to weigh the information they may provide with any risks involved in performing the tests (Table 3).
      Table 3Diagnostic testing for dyspneic patients
      TestGeneral InformationProsCons
      Chest radiographOften primary imagingLow radiation, can assess consolidation, pleural fluid, hyperinflation, pneumothorax, and subcutaneous air. Heart size is apparentLow sensitivity in acute dyspnea. In one series only 8 of 26 pneumonias diagnosed on CT met CXR criteria
      • Syrjala H.
      • Broas M.
      • Suramo I.
      • et al.
      High resolution computed tomography for the diagnosis of community-acquired pneumonia.
      UltrasonographyMultiple protocols to assess acute dyspneaNo radiation, fast, reproducible bedside test, can be done on unstable patients in department and in semirecumbent positionRequires some skill to acquire and interpret bedside images. Patient factors such as subcutaneous air, body habitus, and so forth may limit images
      D-dimerMarker of fibrinolytic activity. When measured by ELISA or second-generation latex agglutination can be used to rule out PE in selected patientsSerum test readily availableRequires risk assessment and clear clinical question. Also increased in consumptive coagulopathy, infection, malignancy, trauma, dissection, preeclampsia, and other cardiovascular disorders
      Arterial blood gasProvides additional information about ventilation (Paco2) to patients with reliable pulse oximetry and bicarbonate level available on BMPMay be faster than general laboratory tests. Useful in assessing anxiety-induced hyperventilation
      • Burri E.
      • Potocki M.
      • Drexler B.
      • et al.
      Value of arterial blood gas analysis in patients with acute dyspnea: an observational study.
      Limited evidence for routine use in undifferentiated dyspnea
      ElectrocardiogramInitial cardiac assessment for assessing dyspneaFast and inexpensive. Easy to compare with prior examinations. Specific for dysrhythmias or ACS limiting perfusionMay be nonspecific in findings such as right heart strain and P pulmonale
      TroponinSerum indicator of myocardial damageSerum test readily availableCan narrow differential to cardiac causes. PE with right heart strain may have increased troponin levels; this finding predicts worse outcomes
      BNP and proBNPUseful in assessing for acute heart failureSerum test readily availableLimited in obesity, mitral regurgitation, flash pulmonary edema, and renal insufficiency. Context is essential
      Complete blood countProvides information about oxygen carrying capacity based on hemoglobin and hematocrit. White blood cell count may indicate infectionSerum test readily availableNonspecific
      CT scanProvides detailed imaging of cardiorespiratory system. Use is increasing, but practitioners should maintain clinical context and consider whether other modalities can answer the clinical questionOffers sensitive and specific resultsSignificant radiation exposure, contrast nephropathy, intravenous contrast dye reactions
      Ventilation/perfusion scanRadiolabeled aerosol and albumin aggregates are used to study ventilation and perfusion. Read as negative or low, medium or high probability for pulmonary embolismLow in radiationLimited by underlying pulmonary disease and availability of isotopes
      Abbreviations: ACS, acute coronary syndrome; BMP, basic metabolic panel; BNP, B-type natriuretic peptide; CT, computed tomography; CXR, chest radiograph; ELISA, enzyme-linked immunosorbent assay; proBNP, pro–B-type natriuretic peptide.
      Ultrasonography provides valuable information about the origin of symptoms, and, often, diagnosis in the initial assessment of an acutely dyspneic patient. These images may be obtained during or shortly after initial assessment, potentially guiding therapy faster than laboratory tests or other imaging studies would be available. The Bedside Lung Ultrasonography in Emergency (BLUE) protocol offers one approach to differentiate several causes of respiratory failure (Table 4 and Fig. 1, Fig. 2, Fig. 3, Fig. 4, Fig. 5, Fig. 6, Fig. 7, Fig. 8, Fig. 9).
      Table 4BLUE protocol
      Adapted from Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest 2008;134(1):117–25; and Courtesy of Petra Duran, MD, RDMS, University of Florida College of Medicine-Jacksonville (FL).
      Ultrasonography FindingUltrasonography ApproachDescriptionClinical MeaningImage
      Assess for artifacts: A linesAnteriorSubpleural air causes repeated linear artifacts parallel to the pleural line (horizontal)Air in lung: either normal or pneumothoraxFig. 1
      Assess for artifacts: B linesAnteriorSeven features: hyperechoic, well-defined, hydroaeric comet-tail artifacts arising from the pleural line. They spread upwards indefinitely and obscure A lines. When lung sliding is present, they move with the lungRepresents an interface of 2 widely different transmissions of ultrasound waves: in this case, air and fluid. When 3 or more B lines are in a single interspace, they are B+ lines (or pulmonary rockets), indicating interstitial syndromeFig. 2
      Assess for lung slidingAnteriorAbsence of lung sliding occurs with a disruption of the normal sliding of viscera on parietal pleura or separation of the two. In M mode, absence of lung slide is seen as the stratosphere sign (also known as bar-code sign)Absence of lung sliding in the presence of A lines necessitates search for pneumothorax. Lung point is the ultrasonography finding in which lung slide is seen in the same view with the abolished lung slide and A lines in the same location, indicating the tip of the lungFig. 3 (stratosphere sign)

      Fig. 4 (normal lung)

      Fig. 5 (lung point)
      Assess for alveolar consolidation or pleural effusion (posterolateral alveolar and/or pleural syndrome)Lateral subposteriorThe classic anechoic, dependent pattern may be inconsistent. Other findings include (1) quad sign: pleural effusion on expiration noted between the pleural and regular, lower lung lines (viscera). (2) Shred sign: tissuelike pattern seen with alveolar consolidation, with the upper border of lung line (or pleural line when there is no effusion) with an irregular lower border. (3) Sinusoid sign: movement of the lung line toward the pleural line in inspirationPleural effusion: sinusoid, plus may have quad sign. Alveolar consolidation: tissuelike appearance or shred sign, absent lung line, absent sinusoidal signFigs. 6 and 7 (pleural effusion)

      Fig. 8 (tissuelike lung)

      Fig. 9 (sinusoidal)
      Deep venous thrombosisFemoral veinsVisualization of thrombus in the lumen or lack of compressibility is positive testConsider pulmonary embolus if positive
      Other protocols include assessments to assess for other cardiac causes of dyspnea.
      • Kajimoto K.
      • Madeen K.
      • Nakayama T.
      • et al.
      Rapid evaluation by lung-cardiac inferior vena cava (LCI) integrated ultrasound for differentiating heart failure from pulmonary disease as the cause of acute dyspnea in the emergency setting.
      • Anderson K.L.
      • Jenq K.Y.
      • Fields J.M.
      • et al.
      Diagnosing heart failure among acutely dyspneic patients with cardiac, inferior vena cava and lung ultrasonography.
      • Russell F.M.
      • Ehrman R.R.
      • Cosby K.
      • et al.
      Diagnosing acute heart failure in patients with undifferentiated dyspnea: a lung and cardiac ultrasound (LuCUS) protocol.
      Focused evaluation of global left ventricular function, diastolic function, right ventricular size, and any pericardial effusion facilitates rapid assessment for massive myocardial infarction, cardiac tamponade, and massive pulmonary embolism at the bedside. In addition, inferior vena cava measurement can be used to assess for right-sided heart failure and to estimate central venous pressure.
      Computed tomography (CT) use to evaluate acute dyspnea has increased in the last decade.
      • Feng L.B.
      • Pines J.M.
      • Yusuf H.R.
      • et al.
      U.S. trends in computed tomography use and diagnoses in emergency department visits by patients with symptoms suggestive of pulmonary embolism, 2001-2009.
      Risks include contrast reactions and nephropathy as well as radiation-induced cancers.
      • Huckins D.S.
      • Price L.L.
      • Gilley K.
      Utilization and yield of chest computed tomographic angiography associated with low positive D-dimer levels.
      Recent American College of Physicians recommendations advocate avoidance of CT as an initial test to evaluate patients at low risk for pulmonary embolism (PE).
      • Qaseem A.
      • Alguire P.
      • Dall P.
      • et al.
      Appropriate use of screening and diagnostic tests to foster, high-value, cost-conscious care.
      Further, nearly one-fourth of patients undergoing CT for PE evaluation have clinically significant incidental findings. Although CT may provide vital diagnostic information, clinicians must not only consider the scan’s necessity but also plan appropriate follow-up for any clinically important incidental findings.
      • Coco A.S.
      • O'gurek D.T.
      Increased emergency department computed tomography use for common chest symptoms without clear patient benefits.
      Always consider whether CT is necessary or whether less risky modalities, such as chest radiograph or ultrasonography, will answer pertinent questions.

      Differential diagnosis for acutely dyspneic patients

      Obstructive Dyspnea

      Consider the 35-year-old woman discussed earlier. Medics report tachypnea with very poor air movement during transport. As she rolls through the ambulance bay doors, you are already assessing her. Adept clinicians can spot respiratory distress from across the room. She is diaphoretic, her shoulders are held adjacent to her ears, and she is breathing extremely rapidly with minimal air movement. You decide to aggressively treat her for a severe asthma exacerbation, starting BIPAP ventilation with continuous nebulized albuterol and order adjunct therapies including intravenous steroids, intravenous magnesium, and intramuscular epinephrine. After 20 minutes at her bedside, she begins to breathe more comfortably with the BIPAP machine and repeat auscultation reveals diffuse wheezing and improved air movement.
      As she begins to improve, EMS returns with another patient. His breath sounds are audible to everyone in the resuscitation bay. He appears diaphoretic and panicked. Examination reveals stridor, periorbital edema, tachycardia, and hypotension. Immediate intervention for anaphylactic shock begins and, after 2 rounds of epinephrine, fluid boluses, antihistamines, and steroids, he too begins to look better.
      Wheezing, or musical respiratory sounds, typically result from partial airway obstruction.
      Chapter 8, The thorax and lungs.
      Because this obstruction can result from inflammation, secretions, or even a foreign body, patients with noisy or whistling breathing need close evaluation to determine whether the noise is inspiratory or expiratory, and whether it is from the lower airways or the upper airways. Stridor from a swollen airway, foreign body, or other airway obstruction is imminently dangerous. Although patients in anaphylaxis may benefit from the nebulized beta-agonist treatment used to treat an asthma exacerbation, it is not sufficient to save their lives. As opposed to wheezing, which is a lower airway expiratory sound, stridor is an upper airway sound transmitted when there is obstruction to the inflow of air during inspiration. The obstruction may be fixed (food bolus; Fig. 10) or inflammatory (anaphylaxis), but in any situation must be emergently managed.
      National and world organizations define asthma “by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation.”

      Global Initiative for Asthma. Diagnosis of diseases of chronic airflow limitation: asthma, COPD and asthma-COPD overlap syndrome (ACOS). 2015. Available at: http://www.ginasthma.org/documents/14/Asthma%2C-COPD-and-Asthma-COPD-Overlap-Syndrome-%28ACOS%29. Accessed May 1, 2015.

      The reversibility of airflow obstruction is the hallmark distinguishing asthma from other obstructive respiratory disorders. In contrast, chronic obstructive pulmonary disease (COPD)/emphysema is defined as “persistent airflow limitation that is usually progressive and associated with enhanced chronic inflammatory responses in the airways and the lungs.”

      Global Initiative for Asthma. Diagnosis of diseases of chronic airflow limitation: asthma, COPD and asthma-COPD overlap syndrome (ACOS). 2015. Available at: http://www.ginasthma.org/documents/14/Asthma%2C-COPD-and-Asthma-COPD-Overlap-Syndrome-%28ACOS%29. Accessed May 1, 2015.

      These patients also frequently wheeze, but may have a different course of acute and chronic disease. Table 5 highlights the differences between these similar, at times overlapping, diseases.
      Table 5Features suggesting asthma or COPD
      Adapted from Global Initiative for Asthma. Diagnosis of diseases of chronic airflow limitation: asthma, COPD and asthma-COPD overlap syndrome (ACOS). 2015. Available at: http://www.ginasthma.org/documents/14/Asthma%2C-COPD-and-Asthma-COPD-Overlap-Syndrome-%28ACOS%29. Accessed May 1, 2015.
      Favors AsthmaFavors COPD
      Onset in childhoodOnset in adulthood
      Symptoms vary over time

      Symptoms worse at night

      Symptoms may be triggered by allergens or exercise
      Symptoms persist even with treatment

      Daily symptoms, some days better than others

      Chronic cough and sputum unrelated to triggers
      Variable airflow obstructionPersistent airflow obstruction
      Normal lung function when asymptomaticAbnormal lung function when asymptomatic
      Atopy in self or familySmoker
      No progression over timeProgression over time
      Asthma is an obstructive disease resulting from increased airway resistance. It is a reversible but recurrent chronic inflammatory disorder that characteristically causes severe dyspnea, wheezing, and coughing.
      • Husain A.N.
      Chapter 15, The lung.
      There are 2 main problems in asthma: chronically inflamed airways and hyperresponsive airways. Intermittent airflow obstruction in symptomatic patients results in decreased ability to expire, leading to hyperinflation, stenting open the alveoli, and increasing the work of breathing. Early in an exacerbation, symptoms are bronchospastic secondary to smooth muscle contraction. As an episode progresses, inflammatory changes in the airways can cause increased airway resistance and lead to VQ mismatch (Fig. 11). The severity of an exacerbation can be assessed clinically and should dictate how aggressively a patient is treated (Table 6).
      Figure thumbnail gr11
      Fig. 11Pathophysiology of symptom development in asthma.
      Table 6Severity of asthma exacerbation assessment
      SymptomsMildModerateSevereNear Death
      BreathlessWhile walkingWhile talkingAt restDecreased effort
      SpeakingIn sentencesIn phrasesIn wordsUnable
      AlertnessMay be agitatedUsually agitatedUsually agitatedConfused
      Respiratory Rate (breaths/min)IncreasedIncreased>30>30, imminent failure
      Accessory Muscle UseUsually notCommonlyUsuallyUsually
      WheezeModerateLoudLoud or silentSilent
      Heart Rate (beats/min)<100100–120>120±
      Saturation (%)>9592–94<90<90
      COPD is defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as “persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.”

      Global Initiative for Asthma. Diagnosis of diseases of chronic airflow limitation: asthma, COPD and asthma-COPD overlap syndrome (ACOS). 2015. Available at: http://www.ginasthma.org/documents/14/Asthma%2C-COPD-and-Asthma-COPD-Overlap-Syndrome-%28ACOS%29. Accessed May 1, 2015.

      The pathophysiology in each patient is typically a mix of lung parenchymal destruction, as seen in emphysema, and small airway inflammation with airway obstruction, or obstructive bronchiolitis.
      Chapter 8, The thorax and lungs.
      An exacerbation of COPD presents as dyspnea, cough, and increased sputum production. In the emergent setting, clinicians must treat the airflow limitation. As with asthma, monitoring of pulse oximetry, degree of respiratory distress, and hemodynamic stability can help clinicians anticipate the degree of severity of a particular exacerbation. More specific testing may also have a role, because radiographs and electrocardiograms may help differentiate other causes of shortness of breath from a COPD exacerbation. In addition, an increase in sputum production or the presence of purulent sputum should be treated with antibiotics, regardless of other infectious symptoms.
      • Ram F.S.
      • Rodriguez-Roison R.
      • Granados-Navarrete A.
      • et al.
      Antibiotics for exacerbations of chronic obstructive pulmonary disease.
      Anaphylaxis is a sudden, potentially fatal, allergic reaction involving multiple organ systems.
      • Sampson H.A.
      • Munoz-Furlong A.
      • Campbell R.L.
      • et al.
      Second Symposium on the Definition and Management of Anaphylaxis: summary Report – Second National Institute of Allergy and Immunology.
      • Simons F.E.S.
      • Ardusso L.R.F.
      • Dimov V.
      • et al.
      World Allergy Organization anaphylaxis guidelines: 2013 update of the evidence base.
      The Second Symposium on the Definition and Management of Anaphylaxis lists the following clinical criteria for diagnosis of anaphylaxis:
      • 1.
        Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (eg, generalized hives; pruritus or flushing; swollen lips, tongue, uvula)
        And at least 1 of the following:
        • a.
          Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced peak expiratory flow, hypoxemia)
        • b.
          Reduced blood pressure (BP) or associated symptoms of end-organ dysfunction (eg, hypotonia [collapse], syncope, incontinence)
      • 2.
        Two or more of the following that occur rapidly after exposure to a likely allergen for that patient:
        • a.
          Involvement of the skin-mucosal tissue
        • b.
          Respiratory compromise
        • c.
          Reduced BP or associated symptoms
        • d.
          Persistent gastrointestinal symptoms (eg, crampy abdominal pain, vomiting)
      • 3.
        Reduced BP after exposure to known allergen for that patient:
        • a.
          Infants and children: low systolic BP (age specific) or greater than 30% decrease in systolic BP
        • b.
          Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from that person’s baseline
      It is the respiratory compromise that is relevant to this article, and it is important to recognize that treating the allergic component of these symptoms is necessary to save the patients.

      Parenchymal Dyspnea

      Now EMS is at the back door with a 60-year-old patient with a history of COPD and congestive heart failure (CHF). He is in respiratory distress with audible wheezing and tripoding. He is diaphoretic, hypertensive, and has pitting edema to his knees. They have given albuterol with no improvement of his symptoms.
      Acute dyspnea is the most common symptom of patients presenting with heart failure.
      • Pang P.S.
      • Collins S.P.
      • Sauser K.
      • et al.
      Assessment of dyspnea early in acute heart failure: patient characteristics and response differences between Likert and visual analog scales.
      Eighty percent of patients with acutely decompensated heart failure present through the ED with a chief complaint of dyspnea.
      • Fonarow G.C.
      The Acute Decompensated Heart Failure National Registry (ADHERE): opportunities to improve care of patients hospitalized with acute decompensated heart failure.
      This symptom is related to both pulmonary and systemic fluid overload and also low cardiac output. American College of Emergency Physicians clinical policy makes level B recommendations that standard clinical judgment can be improved with the use of a single B-type natriuretic peptide (BNP) or N-terminal pro–B-type natriuretic peptide measurement to rule in or out the diagnosis of CHF.
      • Silvers S.M.
      • Howell J.M.
      • Kosowsky J.M.
      • et al.
      Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes.
      However, the true utility, may be in patients with dyspnea not expected to have a CHF exacerbation, when finding a positive BNP would change management and allow a faster initiation of treatment.
      • Carpenter C.R.
      • Keim S.M.
      • Worster A.
      • et al.
      Brain natriuretic peptide in the evaluation of emergency department dyspnea: is there a role?.
      Carpenter and colleagues
      • Carpenter C.R.
      • Keim S.M.
      • Worster A.
      • et al.
      Brain natriuretic peptide in the evaluation of emergency department dyspnea: is there a role?.
      found that the classic constellation of symptoms (jugular venous distension, peripheral edema, rales, and S3) were no more predictive of patients with both pulmonary edema on chest radiograph and an increased BNP level greater than 500 pg/dL than any individual finding alone. Although rales were the most sensitive finding tested for either outcome, they had specificity of only about 50% each. Jugular venous distention and S3 gallop were the individual findings most predictive for pulmonary edema on radiograph or increased BNP level. Ultrasonography measurements of the inferior vena cava also improve diagnostic accuracy versus BNP and chest radiograph alone.
      • Miller J.B.
      • Sen A.
      • Strote S.R.
      • et al.
      Inferior vena cava assessment in the bedside diagnosis of acute heart failure.
      The medics are back in your department, this time with a 75-year-old man with cough and fever. His family is worried that he has been eating less and is sleepier than at hospital discharge last week. In pneumonia, the diffusion of oxygen is limited by alveolar infiltrates, leading to shortness of breath. Common complaints and findings in community-acquired pneumonia include fever, cough, pleuritic chest pain, and sputum production, along with dyspnea. However, these clinical criteria may have a sensitivity as low as 50% compared with a chest radiograph.
      • Metlay J.P.
      • Fine M.J.
      Testing strategies in the initial management of patients with community-acquired pneumonia.
      On examination, many patients have crackles or evidence of consolidation. Guidelines from the Infectious Diseases Society of America and the American Thoracic Society, recommend chest radiograph in patients with suspected pneumonia, which may show lobular consolidation, interstitial infiltrate, or cavitation.
      • Mandell L.A.
      • Wunderink R.G.
      • Anzueto A.
      • et al.
      Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults.
      Although infiltrate with suggestive symptoms makes the diagnosis, infiltrate may not be visible initially on patients with volume depletion. It is appropriate to treat empirically for 24 to 48 hours in these cases and to reimage when hydration is restored.
      The management of pneumonia requires history to allow classification based on the setting in which the illness was acquired. The Infectious Disease Society of America and American Thoracic Society define the types of pneumonia as follows:
      • American Thoracic Society
      • Infectious Diseases Society of America
      Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia.
      Hospital-acquired pneumonia (HAP) is “pneumonia that occurs 48 hours or more after admission which was not incubating at the time of admission.” Ventilator-associated pneumonia (VAP) arises “more than 48-72 hours after endotracheal intubation.” In addition, health care–associated pneumonia (HCAP) is diagnosed in any patient who is “hospitalized in an acute care hospital for two or more days within 90 days of the infection, resided in a nursing home or long-term care facility, received recent IV antibiotic therapy, chemotherapy or wound care within the past 30 days of the current infection or attended a hospital or hemodialysis clinic.” Community-acquired pneumonia is not acquired in any of these situations. These classifications identify typical pathogens and guide appropriate initial management. Important historical exposures and risk factors to refine treatment are summarized in Table 7.
      • Mandell L.A.
      • Wunderink R.G.
      • Anzueto A.
      • et al.
      Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults.
      Table 7Common pathogens in community-acquired pneumonia
      From Mandell LA, Wunderink RG, Anzueto A, et al. Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44(Suppl 2):S46; with permission.
      ConditionCommonly Encountered Pathogens
      AlcoholismStreptococcus pneumoniae, oral anaerobes, Klebsiella pneumoniae, Acinetobacter species, Mycobacterium tuberculosis
      COPD and/or smokingHaemophilus influenzae, Pseudomonas aeruginosa, Legionella species, S pneumonia, Moraxella catarrhalis, Chlamydophila pneumoniae
      AspirationGram-negative enteric pathogens, oral anaerobes
      Lung abscessCA-MRSA, oral anaerobes, endemic fungal pneumonia, M tuberculosis, atypical mycobacteria
      Exposure to bat or bird droppingsHistoplasma capsulatum
      Exposure to birdsChlamydophila psittaci (if poultry: avian influenza)
      Exposure to rabbitsFrancisella tularensis
      Exposure to farm animals or parturient catsCoxiella burnetii (Q fever)
      HIV infection (early)S pneumoniae, H influenzae, M tuberculosis
      HIV infection (late)The pathogens listed for early infection plus Pneumocystis jirovecii, Cryptococcus, Histoplasma, Aspergillus, atypical mycobacteria (especially Mycobacterium kansasii), P aeruginosa, H influenzae
      Hotel or cruise ship stay in previous 2 wkLegionella species
      Travel to or residence in southwestern United StatesCoccidioides species, Hantavirus
      Travel to or residence in southeast and east AsiaBurkholderia pseudomallei, avian influenza, SARS
      Influenza active in communityInfluenza, S pneumoniae, Staphylococcus aureus, H influenzae
      Cough>2 wk with whoop or post-tussive vomitingBordetella pertussis
      Structural lung disease (eg, bronchiectasis)P aeruginosa, Burkholderia cepacia, S aureus
      Injection drug useS aureus, anaerobes, M tuberculosis, S pneumoniae
      Endobronchial obstructionAnaerobes, S pneumonia, H influenzae, S aureus
      In context of bioterrorismBacillus anthracis (anthrax), Yersinia pestis (plague), Francisella tularensis (tularemia)
      Abbreviations: CA-MRSA, community-acquired methicillin-resistant Staphylococcus aureus; HIV, human immunodeficiency virus; SARS, severe acute respiratory syndrome.
      The American Thoracic Society along with the Infectious Disease Society of America’s consensus statement offers 4 important principles in the initial management and evaluation of adult patients with bacterial HAP, VAP, or HCAP; the most important to be accomplished in the ED is to promptly treat with “appropriate and adequate therapy” to decrease mortality.
      • American Thoracic Society
      • Infectious Diseases Society of America
      Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia.

      Circulatory Dyspnea

      After a brief delay, you see a 28-year-old woman with shortness of breath and chest pain. She smokes, uses hormonal birth control, and reports that her symptoms started when she came back from a business trip. Pulmonary embolism (PE) interferes with both ventilation and perfusion. It ultimately causes circulatory collapse because of obstruction of right ventricular outflow eventually causing increased pulmonary artery pressure and failure of the right then left ventricles. Before circulatory collapse, echocardiography can show signs of right ventricular (RV) strain, including dilatation of the right ventricle, RV hypokinesis, paradoxic septal wall motion, McConnell sign (hypokinesis of the free RV wall with sparing of the apex), and tricuspid regurgitation.
      • Kucher N.
      • Rossi E.
      • DeRosa M.
      • et al.
      Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher.
      Dresden and colleagues
      • Dresden S.
      • Mitchell P.
      • Rahimi L.
      • et al.
      Right ventricular dilatation on bedside echocardiography performed by emergency physicians aids in the diagnosis of pulmonary embolism.
      supported the use of ultrasonography in moderate-risk to high-risk patients to determine whether the patients were appropriate for anticoagulation while awaiting definitive imaging. Early anticoagulation is recommended to improve mortality and there is evidence to support anticoagulation before diagnosis in patients with a Wells score greater than 4 who will have a delay to diagnosis of more than 1 hour and 40 minutes.
      • Fesmire F.M.
      • Brown M.D.
      • Espinosa J.A.
      • et al.
      Critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected pulmonary embolism.
      • Blondon M.
      • Righini M.
      • Aujesky D.
      • et al.
      Usefulness of preemptive anticoagulation in patients with suspected pulmonary embolism: a decision analysis.
      The assessment of patients with dyspnea and concern for PE requires a series of risk stratification. One common method is to use Wells criteria
      • Wells P.S.
      • Anderson D.R.
      • Rodger M.
      • et al.
      Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer.
      (Box 1) in patients with suspicion for PE; although other stratification tools exist, none has been shown to be clearly superior. When there is low clinical suspicion for PE, PERC (pulmonary embolism rule-out criteria)
      • Kline J.A.
      • Courtney D.M.
      • Babrhel C.
      • et al.
      Prospective multicenter evaluation of the pulmonary embolism rule-out criteria.
      rules or D-dimer testing may be applied.
      • Fesmire F.M.
      • Brown M.D.
      • Espinosa J.A.
      • et al.
      Critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected pulmonary embolism.
      If PERC (Box 2) is negative, or there is intermediate pretest probability for PE with negative high-sensitivity D-dimer, no further testing for PE is required.
      • Fesmire F.M.
      • Brown M.D.
      • Espinosa J.A.
      • et al.
      Critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected pulmonary embolism.
      When further testing is needed (positive D-dimer or high-sensitivity D-dimer not available), negative CT angiogram or low-probability VQ scan may be used to rule out PE.
      Wells criteria for pulmonary embolism
      • Clinical signs and symptoms of deep vein thrombosis (DVT): +3
      • PE is the main diagnosis or equally likely: +3
      • Heart Rate greater than 100 beats/min: +1.5
      • Immobilization >3 days or surgery in last 4 weeks: +1.5
      • History of prior PE/deep venous thrombosis (DVT): +1.5
      • Hemoptysis: +1
      • Malignancy with treatment within 6 months or palliative: +1
      Less than or equal to 1.5 = low risk, 1.3% chance of PE in ED population; 2 to 6 = moderate risk, 16.2% chance of PE in ED population; greater than 6 = high risk, 40.6% chance of PE in ED population
      Pulmonary embolism rule-out criteria
      • Further work-up recommended if any of the following are present:
        • Age greater than or equal to 50 years
        • Pulse greater than or equal to 100 beats/min
        • Oxygen saturation less than 95%
        • Hemoptysis
        • Unilateral leg swelling
        • History of PE/DVT
        • Exogenous estrogen use
        • Surgery or trauma within 4 weeks that required hospitalization or intubation
      • If none are present, probability of PE is less than 2%.
      In the next bed is a middle-aged woman with diabetes complaining of shortness of breath today. It was associated with some vague nausea and she says that she just does not feel good. Angina pectoris is cardiac chest pain in which oxygen demand outweighs myocardial oxygen supply; in this case caused by occlusion of coronary arteries. Although typically chest pain is a part of the presentation, dyspnea alone may be the initial complaint, termed an anginal equivalent. In one recent large series of patients undergoing stress testing, patients with dyspnea alone were at increased risk of death from cardiac causes. Patients asked simply whether they experienced shortness of breath were considered dyspneic. The subset with no prior known coronary artery disease had more than 4 times the risk of sudden cardiac death versus asymptomatic patients and more than twice the risk of those with typical angina.
      • Abidov A.
      • Rozanski A.
      • Hachamovitch R.
      • et al.
      Prognostic significance of dyspnea in patients referred for cardiac stress testing.
      Clinicians should consider past medical history and risk factors when assessing dyspnea for cardiac causes such as acute myocardial infarction and acute coronary syndrome. Appropriate testing includes bedside electrocardiogram, troponin, and chest radiograph.
      The department eventually settles down and you are able to do some charting until a young man comes in with visible respiratory distress. He is tall and thin, smokes regularly, and reports sudden onset of severely painful breathing. Pneumothorax occurs when air enters the plural space between the chest wall and the lung. Typically only a thin serous layer exists between the visceral and parietal pleura. Air enters this potential space only when there is damage to the lung or chest wall, or a gas-producing pleural space infection. The classic risk factors for bleb rupture causing spontaneous pneumothorax are tall men, although smoking has been suggested to increase the risk of rupture by damaging the pleural layer.
      Pneumothoraces may be identified by ultrasonography, chest radiograph, or CT. Treatment may be guided by cause, severity, comorbidities, interventions such as positive pressure ventilation, size of the pneumothorax, and patient’s preference. Recent studies suggest that uncomplicated spontaneous pneumothorax in patients not undergoing positive pressure ventilation may be treated as successfully with needle aspiration as with other more invasive chest drains, regardless of size.
      • Zehtabchi S.
      • Rios C.L.
      Management of emergency department patients with primary spontaneous pneumothorax: needle aspiration or tube thoracostomy?.
      Tension pneumothorax is a serious event requiring immediate needle decompression to avert loss of cardiac output and arrest. However, recent review shows that the classic presentation of tension pneumothorax with hypotension, absent breath sounds, and deviated trachea may not be immediately seen in patients with spontaneous, unassisted respiration.
      • Roberts D.J.
      • Leigh-smith S.
      • Faris P.D.
      • et al.
      Clinical presentation of patients with tension pneumothorax: a systematic review.
      Because of the slower development of the accumulation of air and pressure variations, spontaneously breathing patients may compensate much longer and present atypically, as shown in Table 8. Thus, clinicians must remain vigilant.
      Table 8Findings in tension pneumothorax
      Adapted from Roberts DJ, Leigh-smith S, Faris PD, et al. Clinical presentation of patients with tension pneumothorax: a systematic review. Ann Surg 2015;261(6):1069.
      Unassisted VentilationPositive Pressure Ventilation
      Spontaneous respiration with air passing through 1-way flapAssisted ventilation forces air through pleural defect into pleural space
      • Compensatory mechanisms delay collapse:
        • Tachycardia and accessory muscle use caused by tachypnea, increased tidal volume, and negative movement of the opposite side of the chest
        • BP is maintained because of limits in the pressure of the pneumothorax on mediastinum and hemithorax
      • Sudden hemodynamic and respiratory compromise:
        • Sedation may increase inspiratory pressure
        • Intrapleural pressure is increased throughout respiratory cycle
      Venous siphon resulting from negative intrathoracic pressure in the opposite side of the chest returns blood to the heartDecreased venous return leads to hypotension and cardiac arrest

      Compensatory Dyspnea

      This article focuses on the cardiopulmonary system as the source of the problem in acutely dyspneic patients. It is important to also consider that the appearance of shortness of breath, tachypnea, or other typical symptoms of dyspnea may result from changing metabolic demands. These patients may appear, on the surface, to be in respiratory distress; they may be tachypneic, tachycardic, even pale or diaphoretic. In these cases, the clinician’s responsibility is to identify and fix the true problem in order to improve the respiratory symptoms.
      Severely anemic patients have limited oxygen carrying capacity. Their bodies therefore experience oxygen hunger, which can manifest as shortness of breath. Patients with dysfunctional hemoglobins secondary to irreversibly bound atoms or toxins may also be functionally anemic with the same symptoms.
      People’s bodies attempt at all costs to maintain equilibrium. Therefore, in metabolic acidoses (such as diabetic ketoacidosis), chemoreceptors detect acidosis and stimulate the respiratory center to hyperventilate. Both the rate and the depth of ventilation often increase, leading to both tachypnea and hyperpnea, at times referred to as Kussmaul respirations. This compensatory response is crucial for survival and should not be mistaken for dyspnea. It is equally important to realize that an increase in alveolar ventilation is not always a compensatory response (to acidosis or to primary pulmonary disorders) and hypocapnia may cause primary respiratory alkalosis, from central nervous system compromise, toxins (eg, salicylates), anxiety, or pain.
      • Morris C.G.
      • Low J.
      Metabolic acidosis in the critically ill: part 1. Classification and pathophysiology.
      In these patients, imaging rarely reveals a source of dyspnea, but clinical suspicion based on history and examination, including signs such as the fruity breath of ketonemia, the pallor of anemia, or the cyanosis of toxic hemoglobinopathies, directs providers toward appropriate laboratory testing and treatment.

      Diagnosis of Exclusion

      In addition, sometimes dyspnea is not dyspnea. Acute anxiety and panic disorder can present as shortness of breath, tachypnea, or hyperventilation. Patients with panic disorder often describe symptoms similar to those of patients with true airway obstruction despite their normal pulmonary function. It has been suggested that these patients have abnormal proprioception, experiencing dyspnea without abnormal stimuli.
      • Smoller J.W.
      • Pollack M.H.
      • Otto M.W.
      • et al.
      Panic anxiety, dyspnea, and respiratory disease.
      However, patients with a history of pulmonary disease can also have pure panic episodes. Arterial blood gas may be useful in diagnosing anxiety-related hyperventilation.
      • Burri E.
      • Potocki M.
      • Drexler B.
      • et al.
      Value of arterial blood gas analysis in patients with acute dyspnea: an observational study.
      Severe pain can also induce abnormal respiratory patterns. Like compensatory problems, pain and anxiety can be managed by managing their causes. Treat pain. Reduce stress and anxiety with words, behaviors, or, if necessary, medications. However, air hunger and difficulty breathing also make individuals anxious. Be sure to avoid premature diagnosis of a purely anxiety-based concern without first evaluating for more dangerous disorders.

      Summary

      Acute dyspnea presents commonly to the ED and it is imperative that emergency physicians be prepared to stabilize patients’ oxygenation and ventilation, which requires careful and efficient consideration of the differential diagnosis. Using cues from the history and physical examination, practitioners may guide the work-up and treatment to identify a parenchymal, obstructive, circulatory, or compensatory cause of dyspnea. Early use of bedside testing, including ultrasonography, may limit unnecessary tests and save time in determining the best treatment course. Thus ensuring both the best care for the patient and also the physician’s ability to readily respond to the next case.

      References

        • Prekker M.E.
        • Feemster L.C.
        • Hough C.L.
        • et al.
        The epidemiology and outcome of prehospital respiratory distress.
        Acad Emerg Med. 2014; 21: 543-550
        • American Thoracic Society
        Dyspnea. Mechanisms, assessment, and management: a consensus statement.
        Am J Respir Crit Care Med. 1999; 159: 321-340
        • Schwartzstein R.M.
        • Lewis A.
        Chapter 29: Dyspnea.
        in: Broaddus V. Mason R.C. Ernst J.D. Murray & Nadel's textbook of respiratory medicine. 6th edition. Elsevier Health Sciences, Saunders/Elsevier, Philadelphia2015: 490-491
        • Kajimoto K.
        • Madeen K.
        • Nakayama T.
        • et al.
        Rapid evaluation by lung-cardiac inferior vena cava (LCI) integrated ultrasound for differentiating heart failure from pulmonary disease as the cause of acute dyspnea in the emergency setting.
        Cardiovasc Ultrasound. 2012; 10: 49
        • Anderson K.L.
        • Jenq K.Y.
        • Fields J.M.
        • et al.
        Diagnosing heart failure among acutely dyspneic patients with cardiac, inferior vena cava and lung ultrasonography.
        Am J Emerg Med. 2013; 31: 1208-1214
        • Russell F.M.
        • Ehrman R.R.
        • Cosby K.
        • et al.
        Diagnosing acute heart failure in patients with undifferentiated dyspnea: a lung and cardiac ultrasound (LuCUS) protocol.
        Acad Emerg Med. 2015; 22: 182-191
        • Feng L.B.
        • Pines J.M.
        • Yusuf H.R.
        • et al.
        U.S. trends in computed tomography use and diagnoses in emergency department visits by patients with symptoms suggestive of pulmonary embolism, 2001-2009.
        Acad Emerg Med. 2013; 20: 1033-1040
        • Huckins D.S.
        • Price L.L.
        • Gilley K.
        Utilization and yield of chest computed tomographic angiography associated with low positive D-dimer levels.
        J Emerg Med. 2012; 43: 211-220
        • Qaseem A.
        • Alguire P.
        • Dall P.
        • et al.
        Appropriate use of screening and diagnostic tests to foster, high-value, cost-conscious care.
        Ann Intern Med. 2012; 156: 147-149
        • Coco A.S.
        • O'gurek D.T.
        Increased emergency department computed tomography use for common chest symptoms without clear patient benefits.
        J Am Board Fam Med. 2012; 25: 33-41
      1. Chapter 8, The thorax and lungs.
        in: Bickley L.S. Szilagyi P.G. Bates’ guide to physical examination and history taking. 11th edition. Lippincott Williams & Wilkins, Philadelphia2013: 301
      2. Global Initiative for Asthma. Diagnosis of diseases of chronic airflow limitation: asthma, COPD and asthma-COPD overlap syndrome (ACOS). 2015. Available at: http://www.ginasthma.org/documents/14/Asthma%2C-COPD-and-Asthma-COPD-Overlap-Syndrome-%28ACOS%29. Accessed May 1, 2015.

        • Husain A.N.
        Chapter 15, The lung.
        in: Kumar V. Abbas A.K. Aster J.C. Robbins and Cotran pathologic basis of disease. 9th edition. WB Saunders, Philadelphia2014: 679
        • Ram F.S.
        • Rodriguez-Roison R.
        • Granados-Navarrete A.
        • et al.
        Antibiotics for exacerbations of chronic obstructive pulmonary disease.
        Cochrane Database Syst Rev. 2006; (CD004403)
        • Sampson H.A.
        • Munoz-Furlong A.
        • Campbell R.L.
        • et al.
        Second Symposium on the Definition and Management of Anaphylaxis: summary Report – Second National Institute of Allergy and Immunology.
        Ann Emerg Med. 2006; 47: 373-380
        • Simons F.E.S.
        • Ardusso L.R.F.
        • Dimov V.
        • et al.
        World Allergy Organization anaphylaxis guidelines: 2013 update of the evidence base.
        Int Arch Allergy Immunol. 2013; 162: 193-204
        • Pang P.S.
        • Collins S.P.
        • Sauser K.
        • et al.
        Assessment of dyspnea early in acute heart failure: patient characteristics and response differences between Likert and visual analog scales.
        Acad Emerg Med. 2014; 21: 659-666
        • Fonarow G.C.
        The Acute Decompensated Heart Failure National Registry (ADHERE): opportunities to improve care of patients hospitalized with acute decompensated heart failure.
        Rev Cardiovasc Med. 2003; 4: S21-S30
        • Silvers S.M.
        • Howell J.M.
        • Kosowsky J.M.
        • et al.
        Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes.
        Ann Emerg Med. 2007; 49: 627-669
        • Carpenter C.R.
        • Keim S.M.
        • Worster A.
        • et al.
        Brain natriuretic peptide in the evaluation of emergency department dyspnea: is there a role?.
        J Emerg Med. 2012; 42: 197-205
        • Miller J.B.
        • Sen A.
        • Strote S.R.
        • et al.
        Inferior vena cava assessment in the bedside diagnosis of acute heart failure.
        Am J Emerg Med. 2012; 30: 778-783
        • Metlay J.P.
        • Fine M.J.
        Testing strategies in the initial management of patients with community-acquired pneumonia.
        Ann Intern Med. 2003; 138: 109
        • Mandell L.A.
        • Wunderink R.G.
        • Anzueto A.
        • et al.
        Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults.
        Clin Infect Dis. 2007; 44: S27-S72
        • American Thoracic Society
        • Infectious Diseases Society of America
        Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia.
        Am J Respir Crit Care Med. 2005; 171: 388-416
        • Kucher N.
        • Rossi E.
        • DeRosa M.
        • et al.
        Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher.
        Arch Intern Med. 2005; 165: 1777-1781
        • Dresden S.
        • Mitchell P.
        • Rahimi L.
        • et al.
        Right ventricular dilatation on bedside echocardiography performed by emergency physicians aids in the diagnosis of pulmonary embolism.
        Ann Emerg Med. 2014; 63: 16-24
        • Fesmire F.M.
        • Brown M.D.
        • Espinosa J.A.
        • et al.
        Critical issues in the evaluation and management of adult patients presenting to the emergency department with suspected pulmonary embolism.
        Ann Emerg Med. 2011; 57: 628-652.e75
        • Blondon M.
        • Righini M.
        • Aujesky D.
        • et al.
        Usefulness of preemptive anticoagulation in patients with suspected pulmonary embolism: a decision analysis.
        Chest. 2012; 142: 697-703
        • Wells P.S.
        • Anderson D.R.
        • Rodger M.
        • et al.
        Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and D-dimer.
        Ann Intern Med. 2001; 135: 98-107
        • Kline J.A.
        • Courtney D.M.
        • Babrhel C.
        • et al.
        Prospective multicenter evaluation of the pulmonary embolism rule-out criteria.
        J Thromb Haemost. 2008; 6: 772-780
        • Abidov A.
        • Rozanski A.
        • Hachamovitch R.
        • et al.
        Prognostic significance of dyspnea in patients referred for cardiac stress testing.
        N Engl J Med. 2005; 353: 1889-1898
        • Zehtabchi S.
        • Rios C.L.
        Management of emergency department patients with primary spontaneous pneumothorax: needle aspiration or tube thoracostomy?.
        Ann Emerg Med. 2008; 51 (100.e1): 91-100
        • Roberts D.J.
        • Leigh-smith S.
        • Faris P.D.
        • et al.
        Clinical presentation of patients with tension pneumothorax: a systematic review.
        Ann Surg. 2015; 261: 1068-1078
        • Morris C.G.
        • Low J.
        Metabolic acidosis in the critically ill: part 1. Classification and pathophysiology.
        Anaesthesia. 2008; 63: 294-301
        • Smoller J.W.
        • Pollack M.H.
        • Otto M.W.
        • et al.
        Panic anxiety, dyspnea, and respiratory disease.
        Am J Respir Crit Care Med. 1996; 154: 6-17
        • Burri E.
        • Potocki M.
        • Drexler B.
        • et al.
        Value of arterial blood gas analysis in patients with acute dyspnea: an observational study.
        Crit Care. 2011; 15: R145
        • Syrjala H.
        • Broas M.
        • Suramo I.
        • et al.
        High resolution computed tomography for the diagnosis of community-acquired pneumonia.
        Clin Infect Dis. 1998; 27: 358-363