Approach to the Patient With Dyspnea

Approach to the patient with dyspneaAuthorRichard M Schwartzstein, MDSection EditorTalmadge E King, Jr, MDDeputy EditorHelen Hollingsworth, MDLast literature review version 18.1: enero 2010 | This topic last updated: septiembre 8, 2009 (More) INTRODUCTIONA consensus statement of the American Thoracic Society defined dyspnea in the following way [1]:"Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses."The American Thoracic Society (ATS) statement on the mechanisms, assessment, and management of dyspnea, as well as other ATS guidelines, can be accessed through the ATS web site at www.thoracic.org/sections/publications/statements/index.html.Dyspnea, or breathing discomfort, is a common symptom that afflicts millions of patients with pulmonary disease and may be the primary manifestation of myocardial ischemia or dysfunction. Examination of the language of dyspnea suggests that this symptom represents a number of qualitatively distinct sensations, and that the words utilized by patients to describe their breathing discomfort may provide insight into the underlying pathophysiology of the disease.The key elements in the evaluation of the patient with acute and chronic dyspnea will be reviewed here with a pathophysiologic construct to guide thinking about a differential diagnosis for the patient with dyspnea. The basic physiology of dyspnea is discussed separately. (See "Physiology of dyspnea".)The majority of patients with chronic dyspnea of unclear etiology have one of four diagnoses [2]: Asthma Chronic obstructive pulmonary disease (COPD) Interstitial lung disease Myocardial dysfunctionPATHOPHYSIOLOGYMost patients with breathing discomfort can be categorized into one of two groups: respiratory system dyspnea or cardiovascular system dyspnea. Respiratory system dyspnea includes discomfort related to disorders of the central controller, the ventilatory pump, and the gas exchanger, while cardiovascular system dyspnea includes cardiac diseases (eg, acute ischemia, systolic dysfunction, valvular disorders, pericardial diseases), anemia, and deconditioning. More than one process may be active in a given patient, and the basic physiology of dyspnea does not always adhere to this structure; for example, stimulation of pulmonary receptors can result from interstitial inflammation (respiratory system) or interstitial edema (cardiovascular system). (See "Physiology of dyspnea".) Nevertheless, this construct offers an organized approach to the patient with dyspnea of unclear etiology.RespiratoryThe respiratory system is designed to move air by bulk transport from the atmosphere to the alveoli, where oxygenis exchanged for carbon dioxide by diffusion across the alveolar-capillary membrane. Carbon dioxide is then removed from the lungs by bulk transport to the atmosphere. Several components must be functioning smoothly for this process to occur; derangements in any of these elements can lead to dyspnea.ControllerThe "respiratory controller" determines the rate and depth of breathing via efferent signals sent to the ventilatory muscles. Factors that stimulate the respiratory centers lead to increased ventilation and breathing discomfort in a variety of settings; these often are secondary to derangements in other parts of the system, such as hypoxia or hypercapnia due to ventilation/perfusion mismatching in the gas exchanger. In addition, drugs such as aspirin(at a toxic dose) or progesteroneand conditions such as pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent of problems in the ventilatory pump or gas exchanger. Typically, dyspnea associated with stimulation of the respiratory controller is described as a sensation of "air hunger" or an "urge or need to breathe" [3-5]. (See "Control of ventilation"and "Physiology of dyspnea".)To some degree, the breathing pattern may also reflect what are presumed to be attempts by the controller to reduce breathing discomfort. Thus, patients with severe airflow obstruction generally adapt a slow, deep breathing pattern to minimize the pleural pressures needed to overcome airways resistance. Alternatively, patients with interstitial fibrosis or kyphoscoliosis and reduced lung or chest wall compliance have a characteristic rapid, shallow breathing pattern which minimizes the work needed to expand the thorax. When the controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation of air hunger. The increase in respiratory rate in the setting of expiratory flow limitation leads to hyperinflation, reduced inspiratory reserve, and increased dyspnea. For any given "drive to breathe," lower tidal volumes are associated with more intense breathing discomfort [4,5].Ventilatory pumpThe "ventilatory pump" is comprised of the ventilatory muscles, the peripheral nerves which transmit signals to them from the controller, the bones of the chest wall to which the respiratory muscles are connected, the pleura which transforms movement of the chest wall to negative pressure inside the thorax, and the airways that serve as a conduit for the flow of gas from the atmosphere to the alveoli and back again. The most common derangements of the ventilatory pump result in a sense of increased "work of breathing" [6-10].Neuromuscular weakness (eg, myasthenia gravis, Guillain-Barr syndrome) leads to a condition in which the patient must exert near maximal inspiratory effort to produce a normal negative pleural pressure [11]. Patients with reduced compliance of the chest wall (eg, kyphoscoliosis) or lungs (eg, interstitial fibrosis) must perform more work than normal to move air into the lungs. Obstructive lung disease is associated with increased resistance to flow and, in patients with significant hyperinflation, reduced compliance as breathing occurs on the stiff portion of the pressure-volume curve of the respiratory system. When hyperinflation results in an end-inspiratory volume that approximates total lung capacity, patients often complain of an inability to get a deeper satisfying breath [9]. A sensation of chest tightness may also be present in patients in whom acute bronchoconstriction is the cause of airflow obstruction [6,7,12,13].Gas exchangerThe "gas exchanger" consists of the alveoli and the pulmonary capillaries across which oxygenand carbon dioxide diffuse. Most of the common cardiopulmonary disorders leading to dyspnea are associated with some derangement of the gas exchanger due either to destruction of the diffusing membrane (eg, emphysema, pulmonary fibrosis) or the imposition of fluid or inflammatory material between the capillaries and the gas in the alveoli. Diseases affecting the gas exchanger are typically characterized by hypoxemia, either at rest or with exercise, and by chronic hypercapnia in more severe cases. These gas exchange abnormalities stimulate the respiratory centers in the brainstem and lead to a sensation of "air hunger" or an increased urge to breathe.CardiovascularThe cardiovascular system is designed to move oxygenated blood from the lungs to metabolically active tissues, and then transport carbon dioxide from the tissues back to the lungs. For this system to work optimally and avert breathing discomfort, one must have a pump that functions without generating high pulmonary capillary pressures. There must also be sufficient hemoglobin to carry oxygenand appropriate enzymes to utilize oxygen in the tissues.Heart failureHeart failure is a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle(s) to fill with or eject blood. Symptoms of heart failure fall into two major classes: those due to a reduction in cardiac output (fatigue, weakness) and those due to increased pulmonary or systemic venous pressure and fluid accumulation (dyspnea, edema, hepatic congestion, and ascites). When heart failure causes an increase in pulmonary venous pressure, it can lead to dyspnea either by producing hypoxemia or by stimulating pulmonary vascular and/or interstitial receptors (eg, unmyelinated J-receptors, also called C-fibers). Causes of heart failure include ventricular systolic dysfunction, ventricular diastolic dysfunction, and valvular disease. Cardiac tamponade may also lead to dyspnea by increasing pulmonary vascular pressures. (See "Physiology of dyspnea"and "Evaluation of the patient with suspected heart failure"and "Cardiac tamponade".)AnemiaAnemia can severely impair oxygendelivery because the bulk of oxygen carried in the blood is hemoglobin-bound. (See "Structure and function of normal human hemoglobins".) Nevertheless, the exact mechanism by which anemia produces dyspnea is unknown. To the extent that the local pH of metabolically active cells decreases due to the inability to sustain aerobic metabolism, there may be stimulation of "ergoreceptors" which are believed to be located in the muscles and which respond to such changes in the microenvironment of the cell [14,15]. Anemia also leads to increased cardiac output, which may necessitate elevated left ventricular volume and pulmonary vascular pressures. However, the quality of dyspnea is usually quite different in these two clinical situations.DeconditioningIndividuals usually complain of respiratory discomfort when they engage in vigorous physical activity, even in the presence of a normal cardiovascular and respiratory system and normal hematocrit. More fit individuals experience less discomfort for any given workload; cardiovascular fitness is determined by the ability of the heart to increase maximal cardiac output and by the ability of the peripheral muscles to utilize oxygenefficiently for aerobic metabolism.In contrast, a sedentary existence reduces fitness and leads to dyspnea, often with seemingly trivial tasks. It is common for patients with chronic cardiopulmonary disease to assume a sedentary lifestyle in an effort to avoid breathing discomfort. However, the end result over a span of months to years is that the individual becomes progressively deconditioned and ultimately may be limited more by poor cardiovascular fitness than by the underlying disease [16]. Dyspnea due to deconditioning is typically described as "heavy breathing" or a sense of "breathing more" [8], and with careful questioning, one can determine that the patient is actually limited by fatigue rather than breathing discomfort.LANGUAGE OF DYSPNEAWhen eliciting a history from a patient presenting with a complaint of pain, clinicians are taught to always inquire about the quality of the pain. As an example, chest pain may mean very different things if it is described as "sharp," "burning," or "crushing." (see "Management of suspected acute coronary syndrome in the emergency department"section on Characteristic history and associated symptoms.) .In the 1970s and 1980s a number of pain questionnaires were developed [17,18], and studies in which they were utilized for headache and facial pain demonstrated that clinicians could draw inferences about the cause of these symptoms depending upon the responses of a given patient [19,20].The notion that pain is comprised of multiple, qualitatively distinct sensations comes easily to most clinicians because everyone experiences a range of painful sensations as part of normal living (eg, headaches, stomach aches, tooth pain, burns, bruises, etc). However, if one has a normal cardiopulmonary system, the only dyspnea one is likely to experience is that which occurs with heavy exercise. This makes it more difficult for the average examiner to question a patient with breathing discomfort in a way that captures the subtleties of asthma, heart failure, COPD, or pulmonary embolism [21].QuestionnairesThe first dyspnea questionnaires were developed in the late 1980s based upon informal data obtained from patients and the systematic questioning of normal subjects made breathless by the imposition of a range of respiratory tasks [3]. These tasks including breathing when resistive or elastic loads were added, when end-expiratory lung volume was changed, when tidal volume was restricted, or when carbon dioxide was inhaled. In these settings, the sensations of respiratory discomfort produced by the different causes of dyspnea were different and easily distinguishable.As a result of these studies, clusters of terms emerged that were allied with one or another of the respiratory tasks. Similar dyspnea questionnaires were then presented to patients with breathing discomfort from a variety of cardiopulmonary disorders (table 1)[6-8,22]. Subjects were asked to select the phrases that best described their breathing discomfort, and distinct clusters again emerged. While some clusters of phrases were common to a number of disease categories (eg, increased work or effort of breathing was found with COPD, asthma, and neuromuscular disease), each disease had a relatively unique set of clusters associated with it.These data suggested that the physiologic mechanisms responsible for dyspnea in each patient group are likely to have some elements in common, and some that are unique. Attention to the words that patients use in describing their breathing discomfort may provide insight into the underlying clinical condition as well as the basic physiologic mechanisms producing dyspnea.Research in this area is continuing, and one incompletely resolved issue is the potential role that ethnicity and cultural context play in influencing an individual's description of dyspnea. Studies using dyspnea questionnaires in the United States [6,8]and the United Kingdom [8]have demonstrated similar sensory descriptions across a number of disease states. On the other hand, one study of 32 patients with asthma found significant differences among African-American and white subjects in their use of descriptors [23]. However, in this investigation, subjects were not given a questionnaire nor were they asked to describe their breathing discomfort; rather, they offered spontaneous comments about any sensations associated with inhalation of methacholine. Research confirms the utility of studying the qualities of dyspnea in different languages [24,25]. The cross-cultural generalizability of specific dyspnea questionnaires is uncertain.Using questionnairesMost studies of the language of dyspnea have been performed in patients with known cardiopulmonary disorders or in normal subjects made breathless under experimental conditions. These indicate the following (table 2)[21]: Acute hypercapnia or restricted thoracic motion produces a sensation of "air hunger" [4,5,26]. Acute bronchoconstriction leads to a series of sensations from "chest tightness" to an increased "effort to breathe" to a sensation of "air hunger" as the degree of obstruction worsens [6-8,12,13]. The sensation of "tightness" appears to be independent of the work of breathing [27].One study explored the use of dyspnea questionnaires in evaluating patients receiving treatment for acute bronchoconstriction [10]. Patients undergoing bronchodilator therapy in an emergency department reported decreased breathing discomfort in association with relief of their "chest tightness." However, the sense of increased "effort" to breathe persisted, as did moderate spirometric airflow obstruction.This study may provide insight into the different components of dyspnea in asthma: chest tightness relieved by bronchodilators may reflect changes in pulmonary receptor activation as bronchospasm diminishes, while the effort of breathing relates to ongoing airflow obstruction and/or hyperinflation remaining due to airways inflammation.Attention to the use of verbal descriptors in such patients may help the clinician avoid underestimation of the severity of asthma when objective measurements of lung function are not possible. Patients with COPD complain of an increased "effort to breathe" as well as a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. Heart failure is associated with a sensation of "air hunger" and "suffocation" [6]. Cardiovascular deconditioning is characterized by "heavy breathing" [8].Prospective studies examining the clinical utility of dyspnea questionnaires are underway. We have had extensive experience using these tools in patients referred for evaluation of chronic dyspnea and have found them to be helpful, particularly in patients with more than one cardiopulmonary disorder and in patients in whom dyspnea appears out of proportion to their underlying lung disease. As an example, a patient with sarcoidosis who experienced worsening shortness of breath was increasing her dose of oral corticosteroidson the presumption that her parenchymal disease was flaring, but was found to have superimposed airways reactivity after she selected "chest tightness" as the phrase that best described her breathing discomfort. Similarly, a patient with COPD who had significant functional constraints presumed due to his emphysema was found to be limited primarily by cardiovascular deconditioning when he noted that his dyspnea with exertion was best described as "heavy breathing." He denied the qualities of dyspnea most typical of COPD (difficulty moving air in or out of his lungs or a sensation of not being able to get a deep breath).ACUTE DYSPNEABreathing discomfort arising over the course of minutes to hours is due to a relatively limited number of conditions (table 3). These entities typically have associated symptoms and signs that provide clues to the appropriate diagnosis, eg, substernal chest pain with cardiac ischemia; fever, cough, and sputum with respiratory infections; urticaria with anaphylaxis; and wheezing with acute bronchospasm. However, dyspnea may be the sole complaint and the physical examination may reveal few abnormalities (eg, pulmonary embolism, pneumothorax). In these cases, attention to historical information and a review of this limited differential diagnosis are important. (See "Evaluation of the adult with dyspnea in the emergency department".)Plasma BNPThe symptoms and physical findings of heart failure (HF) can be subtle; however, establishing HF as the etiology of a patient's dyspnea is extremely important because management will be altered. With chronic and advanced HF, ventricular cells are recruited to secrete atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in response to the high ventricular filling pressures. As a result, the plasma concentrations of both hormones are increased in patients with asymptomatic and symptomatic left ventricular dysfunction, making them useful diagnostic markers.With the rapid bedside assay for BNP, most dyspneic patients with HF have values above 400 pg/mL, while left ventricular dysfunction without exacerbation, pulmonary embolism, and cor pulmonale should be considered in dyspneic patients with plasma BNP concentrations between 100 and 400 pg/mL (graph 1)[28,29]. The value of plasma BNP and its precursor, N-terminal pro-BNP, in distinguishing HF from other causes of dyspnea is discussed in detail separately. (See "Evaluation of the patient with suspected heart failure", section on 'BNP and NT-proBNP'and "Brain natriuretic peptide measurement in left ventricular dysfunction and other cardiac diseases", section on 'Plasma BNP in heart failure'.)CHRONIC DYSPNEAThe etiology of dyspnea may prove elusive when it develops over weeks to months. Patients commonly have known cardiopulmonary disease, but symptoms are out of proportion to demonstrable physiologic impairments. A majority of patients with dyspnea of unclear cause have one of four etiologies: asthma, COPD, interstitial lung disease, or cardiomyopathy [2].In one study of 85 patients presenting to a pulmonary unit with a complaint of chronic dyspnea, the initial impression of the etiology of dyspnea based upon the patient history alone was correct in only 66 percent of cases [2]. Thus, a systematic approach to these patients is necessary.History and physical examinationAs noted above, attention to the quality of the breathing discomfort often provides clues to the underlying diagnosis: Chest tightness may be indicative of bronchospasm A sensation of rapid, shallow breathing may correspond to interstitial disease A sense of heavy breathing is typical of deconditioningThe history may reveal other valuable clues. The absence of cigarette smoking argues strongly against a diagnosis of chronic obstructive pulmonary disease. The occupational history may lead to a diagnosis of asbestosis or hypersensitivity pneumonitis. The presence of specific, reproducible inciting events such as exposure to fumes or cold air is common with airways hyperreactivity. However, a known chronic cardiopulmonary disease does not guarantee that the patient's symptoms are due to that condition [16]. The rapidity with which symptoms develop during exercise can also provide useful diagnostic information. For example, patients who develop acute elevations in pulmonary capillary wedge pressure generally develop shortness of breath and wheezing within 50 to 100 feet. In contrast, symptoms of exercise-induced asthma usually are precipitated by more intense activity. (See "Exercise-induced bronchoconstriction".)In general, the negative predictive value of absent physical findings is higher than the positive predictive value for signs obtained from the examination of patients with chronic dyspnea [2].Laboratory and radiographic testingThe initial evaluation following the history and physical examination should include a hematocrit (to exclude anemia as a contributing factor to respiratory discomfort), a chest radiograph, spirometry, and oximetry during ambulation at a normal pace over approximately 200 meters.The chest radiograph may provide evidence of hyperinflation and bullous disease suggestive of obstructive lung disease, or changes in interstitial markings consistent with inflammation or interstitial fluid. Abnormalities of heart size may indicate valvular disease or other cardiac dysfunction. Echocardiography is reserved for patients in whom the heart is enlarged on chest radiograph or in whom the diagnosis of chronic thromboembolic disease or pulmonary hypertension is being considered.Spirometry provides data on airway function and can suggest an underlying "restrictive" abnormality that could be confirmed with measurement of lung volumes. Complete pulmonary function testing with assessment of lung volumes and diffusing capacity is generally reserved for individuals in whom interstitial fibrosis is being considered, in those who have significant declines in oxygensaturation with exercise, or in those for whom there is a question of ventilatory muscle weakness. (See "Overview of pulmonary function testing in adults"and "Diffusing capacity for carbon monoxide".)Computed tomography (CT) of the chest usually is not indicated in the initial evaluation of patients with dyspnea, but can be valuable in three circumstances: A small percentage of patients with pulmonary fibrosis may have a normal chest radiograph on presentation; CT scan clearly is more sensitive for detecting mild degrees of alveolitis [30,31]. Thus, patients with crackles on physical examination or reduced lung volumes on pulmonary function testing should have CT scans if the chest radiograph is normal. A minority of patients with a history of cigarette smoking, normal spirometry, and normal chest radiographs have extensive emphysema on high-resolution CT scan [32]. These patients generally demonstrate oxygendesaturation with exercise and have a low diffusing capacity. In patients in whom chronic thromboembolic disease is a consideration due to elevation of pulmonary artery pressure on an echocardiogram or oxygendesaturation during exercise.Cardiopulmonary exercise testingCardiopulmonary exercise testing is indicated when the etiology of a patient's dyspnea remains unclear after the initial evaluation described above, or when it seems out of proportion to the severity of the patient's known cardiac or pulmonary disease. This testing, during which a range of physiologic parameters is monitored, allows one to determine if the patient's dyspnea is more likely due to cardiovascular or respiratory system abnormalities. (See "Functional exercise testing: Ventilatory gas analysis"and "Exercise physiology".)Cardiopulmonary exercise testing is particularly helpful in establishing the diagnosis of deconditioning and can yield clues about the presence of primary hyperventilation syndromes. The technique also detects patients with a low threshold for respiratory discomfort; these individuals terminate the test at mild workloads because of dyspnea but have no evidence of cardiopulmonary abnormality.BEHAVIORAL CONSIDERATIONSA symptom is the end result of a sequence of events that begins with stimulation of one or more receptors, leads to the transmission of neural information from those receptors to the brain, and ultimately involves the processing of that information so that it becomes a perception. An individual's education, experience, and behavioral style are important in shaping the ultimate perception of a given stimulus [33,34].The global rating that a patient gives for dyspnea may reflect both sensory and emotional (ie, affective) elements. In a study of laboratory-induced dyspnea, air hunger was associated with greater unpleasantness for a given level of sensory intensity than was the sense of respiratory work or effort [35]. The context in which a sensation occurs may alter the affective component of the intensity and needs to be considered when assessing the patient.For a given physiologic derangement, eg, a drop in FEV1 or PaO2, there is a wide range of perceptual responses among individuals. Anxiety, anger, pain, and depression may be associated with dyspnea intensity out of proportion to the physiologic impairment [36-39]. 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 respiratory discomfort for any given activity.SUMMARY AND RECOMMENDATIONSDyspnea can be the first manifestation of a variety of cardiopulmonary disorders. We recommend the following approach when evaluating a patient with dyspnea of unclear etiology or dyspnea out of proportion to known physiologic abnormalities: When developing a differential diagnosis, use a construct that distinguishes respiratory system dyspnea from cardiovascular dyspnea. It is not uncommon for a patient to have more than one problem contributing to the breathing discomfort. The most common causes of chronic dyspnea are asthma, COPD, interstitial lung disease, and cardiomyopathy, but deconditioning is often a major contributing factor in patients with chronic lung disease (see 'Pathophysiology'above). Inquire about the quality of the patient's breathing discomfort and attempt to ascertain whether the individual has more than one type of discomfort under different conditions. Use of dyspnea questionnaires can be helpful in eliciting this information from patients with chronic dyspnea (see 'Language of dyspnea'above). Plasma brain natriuretic peptide (BNP) levels may be helpful in establishing or excluding the diagnosis of heart failure as a cause of acute dyspnea (see 'Acute dyspnea'above). The history and physical examination lead to accurate diagnoses in patients with dyspnea in approximately two-thirds of cases; chest radiography and pulmonary function testing should be the first tests obtained in the majority of cases in which additional information is required. CT scanning is generally reserved for patients in whom there is a suspicion of interstitial lung disease, occult emphysema, or chronic thromboembolic disease. (See 'Laboratory and radiographic testing'above.) Cardiopulmonary exercise testing is a useful study in patients in whom the cause of their breathing discomfort remains elusive after standard testing, in patients in whom deconditioning is a serious consideration, and in patients who appear to have breathing discomfort out of proportion to their physiologic derangements. 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Evaluation of the adult with dyspnea in the emergency departmentAuthorsAzeemuddin Ahmed, MD, FACEPMark A Graber, MD, FACEPEric W Dickson, MD, MHCM, FACEPSection EditorRobert S Hockberger, MD, FACEPDeputy EditorJonathan Grayzel, MD, FAAEMLast literature review version 18.1: enero 2010 | This topic last updated: septiembre 21, 2009 (More) INTRODUCTIONDyspnea 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.PATHOPHYSIOLOGYThe 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".)EPIDEMIOLOGYDyspnea 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