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A consensus statement of the American Thoracic Society defines 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."

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pnea" and "Evaluation of the adult with dyspnea in the emergency department" and "Maternal adaptations to pregnancy: Dyspnea and other physiologic respiratory changes".) DEFINITION OF DYSPNEA — <span>A consensus statement of the American Thoracic Society defines 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." Dyspnea is considered acute when it develops over hours to days and chronic when it occurs for more than four to eight weeks. Some patients present with acute worsening of chronic breat




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Dyspnea is considered acute when it develops over hours to days and chronic when it occurs for more than four to eight weeks.
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nsity. The experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses." <span>Dyspnea is considered acute when it develops over hours to days and chronic when it occurs for more than four to eight weeks. Some patients present with acute worsening of chronic breathlessness that may be caused by a new problem or a worsening of the underlying disease (eg, asthma, chronic obstructive pulmon




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Most 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 (table 1), while cardiovascular system dyspnea includes cardiac diseases (eg, acute ischemia, systolic dysfunction, valvular disorders, pericardial diseases), anemia, and deconditioning (figure 1)
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) 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/statements. PATHOPHYSIOLOGY — <span>Most 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 (table 1), while cardiovascular system dyspnea includes cardiac diseases (eg, acute ischemia, systolic dysfunction, valvular disorders, pericardial diseases), anemia, and deconditioning (figure 1). 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 ca




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Factors that stimulate the respiratory centers in the brainstem 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, or stimulation of pulmonary receptors as occurs with interstitial inflammation or edema
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gements in any of these elements can lead to dyspnea. ●Controller – The "respiratory controller" determines the rate and depth of breathing via efferent signals sent to the ventilatory muscles. <span>Factors that stimulate the respiratory centers in the brainstem 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, or stimulation of pulmonary receptors as occurs with interstitial inflammation or edema. In addition, drugs such as aspirin (at a toxic dose) or progesterone and conditions such as pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent o




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In addition, drugs such as aspirin (at a toxic dose) or progesterone and conditions such as pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent of problems in the ventilatory pump or gas exchanger.
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he system, such as hypoxia or hypercapnia due to ventilation/perfusion mismatching in the gas exchanger, or stimulation of pulmonary receptors as occurs with interstitial inflammation or edema. <span>In addition, drugs such as aspirin (at a toxic dose) or progesterone and 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" [2-4]. (See "Control of ventilat




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Typically, dyspnea associated with stimulation of the respiratory controller is described as a sensation of "air hunger" or an "urge or need to breathe" [2-4]
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xic dose) or progesterone and conditions such as pregnancy or diabetic ketoacidosis can produce dyspnea through central effects independent of problems in the ventilatory pump or gas exchanger. <span>Typically, dyspnea associated with stimulation of the respiratory controller is described as a sensation of "air hunger" or an "urge or need to breathe" [2-4]. (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 breathin




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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 relatively 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
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ted with stimulation of the respiratory controller is described as a sensation of "air hunger" or an "urge or need to breathe" [2-4]. (See "Control of ventilation" and "Physiology of dyspnea".) <span>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 relatively 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 respiratory controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation of air hunger. The increase in respiratory rate during exercise in the s




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When the respiratory controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation of air hunger. The increase in respiratory rate during exercise in the setting of expiratory flow limitation can lead to exercise-induced air-trapping, a process known as dynamic hyperinflation. Dynamic hyperinflation is associated with a reduced inspiratory reserve and increased dyspnea. For those in whom hyperinflation is substantial, such that inspiratory capacity at rest or during exercise is limited by total lung capacity, dyspnea is further exacerbated, and patients may also complain of an inability to get a deep breath.
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th 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. <span>When the respiratory controller is stimulated (eg, by exercise), airflow obstruction may heighten the sensation of air hunger. The increase in respiratory rate during exercise in the setting of expiratory flow limitation can lead to exercise-induced air-trapping, a process known as dynamic hyperinflation. Dynamic hyperinflation is associated with a reduced inspiratory reserve and increased dyspnea. For those in whom hyperinflation is substantial, such that inspiratory capacity at rest or during exercise is limited by total lung capacity, dyspnea is further exacerbated, and patients may also complain of an inability to get a deep breath. (See "Dynamic hyperinflation in patients with COPD".) For patients with restrictive lung disease, the adoption of breathing patterns with either an increase or decrease in tidal volume




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For patients with restrictive lung disease, the adoption of breathing patterns with either an increase or decrease in tidal volume from their average resting tidal volume results in increased dyspnea [5]. Breathing with a rapid, shallow pattern, the patient experiences an increase in the ratio of dead space to tidal volume (since anatomic dead space is relatively fixed), which leads to a need for greater total ventilation (hence, the increase in respiratory rate); this adds to respiratory work-load and may contribute to the development of hypercapnia. In contrast, an increase in tidal volume requires a significant increase in respiratory work due to the stiffness of the lung. Since most patients with restrictive lung disease tend to use a rapid, shallow breathing pattern, we conclude that this pattern, relative to alternatives, must produce less dyspnea
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ise is limited by total lung capacity, dyspnea is further exacerbated, and patients may also complain of an inability to get a deep breath. (See "Dynamic hyperinflation in patients with COPD".) <span>For patients with restrictive lung disease, the adoption of breathing patterns with either an increase or decrease in tidal volume from their average resting tidal volume results in increased dyspnea [5]. Breathing with a rapid, shallow pattern, the patient experiences an increase in the ratio of dead space to tidal volume (since anatomic dead space is relatively fixed), which leads to a need for greater total ventilation (hence, the increase in respiratory rate); this adds to respiratory work-load and may contribute to the development of hypercapnia. In contrast, an increase in tidal volume requires a significant increase in respiratory work due to the stiffness of the lung. Since most patients with restrictive lung disease tend to use a rapid, shallow breathing pattern, we conclude that this pattern, relative to alternatives, must produce less dyspnea. ●Ventilatory pump – The "ventilatory pump" comprises the ventilatory muscles, the peripheral nerves which transmit signals to them from the controller, the bones of the chest wall to w




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The "ventilatory pump" comprises 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].
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st patients with restrictive lung disease tend to use a rapid, shallow breathing pattern, we conclude that this pattern, relative to alternatives, must produce less dyspnea. ●Ventilatory pump – <span>The "ventilatory pump" comprises 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-Barré syndrome) leads to a condition in which the patient must exert near maximal inspiratory effort to produce a normal negative




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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].
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ncreased 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. <span>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 exchanger – The "gas exchanger" consists of the alveoli and the pulmonary capillaries across which oxygen and carbon dioxide diffuse. Most of the common cardiopulmonary disorders l




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Neuromuscular weakness (eg, myasthenia gravis, Guillain-Barré 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
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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]. <span>Neuromuscular weakness (eg, myasthenia gravis, Guillain-Barré 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 sensati




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The "gas exchanger" consists of the alveoli and the pulmonary capillaries across which oxygen and 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 addition of fluid or inflammatory material into the lungs such that ventilation to alveoli is reduced regionally. To a lesser degree, the distance for diffusion may also contribute in these conditions or in the greatly dilated pulmonary capillaries seen in some patients with hepatopulmonary syndrome. Diseases affecting the gas exchanger are typically characterized by hypoxemia, either at rest or with exercise, and by chronic hypercapnia in more severe cases
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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 exchanger – <span>The "gas exchanger" consists of the alveoli and the pulmonary capillaries across which oxygen and 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 addition of fluid or inflammatory material into the lungs such that ventilation to alveoli is reduced regionally. To a lesser degree, the distance for diffusion may also contribute in these conditions or in the greatly dilated pulmonary capillaries seen in some patients with hepatopulmonary syndrome. 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. Cardiovascular — The cardio




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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 oxygen and appropriate enzymes to utilize oxygen in the tissues.
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iovascular — The 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. <span>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 oxygen and appropriate enzymes to utilize oxygen in the tissues. ●Heart failure – Heart 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 eje




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Symptoms of heart failure fall into two major classes: those due to a reduction in cardiac output (fatigue, weakness, and dyspnea on exertion) and those due to increased pulmonary or systemic venous pressure and fluid accumulation (dyspnea at rest and exertion, edema, hepatic congestion, and ascites)
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Heart failure – Heart 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. <span>Symptoms of heart failure fall into two major classes: those due to a reduction in cardiac output (fatigue, weakness, and dyspnea on exertion) and those due to increased pulmonary or systemic venous pressure and fluid accumulation (dyspnea at rest and exertion, 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 recept




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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)
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eakness, and dyspnea on exertion) and those due to increased pulmonary or systemic venous pressure and fluid accumulation (dyspnea at rest and exertion, edema, hepatic congestion, and ascites). <span>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 pulm




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In patients with low cardiac output, oxygen delivery to the tissues is reduced, which may lead to changes in tissue metabolism with associated accumulation of products of anaerobic energy generation leading to stimulation of metabo- or ergoreceptors [14,15], which can lead to dyspnea.
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may also lead to dyspnea by increasing pulmonary vascular pressures. (See "Physiology of dyspnea" and "Heart failure: Clinical manifestations and diagnosis in adults" and "Cardiac tamponade".) <span>In patients with low cardiac output, oxygen delivery to the tissues is reduced, which may lead to changes in tissue metabolism with associated accumulation of products of anaerobic energy generation leading to stimulation of metabo- or ergoreceptors [14,15], which can lead to dyspnea. ●Anemia – Anemia can severely impair oxygen delivery because the bulk of oxygen carried in the blood is hemoglobin-bound (see "Structure and function of normal hemoglobins"). Neverthele




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Anemia can severely impair oxygen delivery because the bulk of oxygen carried in the blood is hemoglobin-bound (see "Structure and function of normal hemoglobins"). Nevertheless, the exact mechanism by which anemia produces dyspnea is not known.
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ges in tissue metabolism with associated accumulation of products of anaerobic energy generation leading to stimulation of metabo- or ergoreceptors [14,15], which can lead to dyspnea. ●Anemia – <span>Anemia can severely impair oxygen delivery because the bulk of oxygen carried in the blood is hemoglobin-bound (see "Structure and function of normal hemoglobins"). Nevertheless, the exact mechanism by which anemia produces dyspnea is not known. As described above for low cardiac output heart failure, the inability to sustain aerobic metabolism may lead to stimulation of "ergoreceptors" [14,15]. Anemia also leads to increased c




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Individuals 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 oxygen efficiently for aerobic metabolism.
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may necessitate elevated left ventricular volume and pulmonary vascular pressures. However, the quality of dyspnea is usually quite different in these two clinical situations. ●Deconditioning – <span>Individuals 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 oxygen efficiently 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 s




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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 (ie, reduced maximal cardiac output, reduced capillary density in the muscles, and reduced mitochondrial capacity to sustain aerobic metabolism) and ultimately may be limited more by poor cardiovascular fitness than by the underlying disease [16].
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lity of the peripheral muscles to utilize oxygen efficiently for aerobic metabolism. In contrast, a sedentary existence reduces fitness and leads to dyspnea, often with seemingly trivial tasks. <span>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 (ie, reduced maximal cardiac output, reduced capillary density in the muscles, and reduced mitochondrial capacity to sustain aerobic metabolism) 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 actuall




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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 or leg discomfort rather than breathing discomfort.
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density in the muscles, and reduced mitochondrial capacity to sustain aerobic metabolism) and ultimately may be limited more by poor cardiovascular fitness than by the underlying disease [16]. <span>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 or leg discomfort rather than breathing discomfort. CLINICAL ASSESSMENT — While clinical history is often insufficient to make a secure diagnosis, it provides guidance in narrowing the diagnostic possibilities and selecting diagnostic te




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While clinical history is often insufficient to make a secure diagnosis, it provides guidance in narrowing the diagnostic possibilities and selecting diagnostic tests. 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 [17]. Thus, a systematic diagnostic approach to these patients is necessary.
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f "breathing more" [8], and with careful questioning, one can determine that the patient is actually limited by fatigue or leg discomfort rather than breathing discomfort. CLINICAL ASSESSMENT — <span>While clinical history is often insufficient to make a secure diagnosis, it provides guidance in narrowing the diagnostic possibilities and selecting diagnostic tests. 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 [17]. Thus, a systematic diagnostic approach to these patients is necessary. Temporal pattern and triggers — The temporal pattern of breathlessness and association with certain triggers can provide important clues. Breathing discomfort arising over the course of




#Diagnostic #Dyspnea #Dyspnee #Dyspnée #GarjoDyspnee #Pneumologie #Semiologie #U2D
The temporal pattern of breathlessness and association with certain triggers can provide important clues. Breathing discomfort arising over the course of minutes to hours is due to a relatively limited number of conditions (table 2). These entities typically have associated symptoms and signs that provide clues to the appropriate diagnosis
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dyspnea based upon the patient history alone was correct in only 66 percent of cases [17]. Thus, a systematic diagnostic approach to these patients is necessary. Temporal pattern and triggers — <span>The temporal pattern of breathlessness and association with certain triggers can provide important clues. Breathing discomfort arising over the course of minutes to hours is due to a relatively limited number of conditions (table 2). 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, dyspne




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Chronic exertional dyspnea and paroxysmal nocturnal dyspnea (PND) are both associated with heart failure, although nocturnal dyspnea is more specific to heart failure. Asthma is also associated with exertional and nocturnal dyspnea, but unlike PND does not usually improve with sitting or standing.
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are important. The approach to acute dyspnea is described separately. (See "Evaluation of the adult with dyspnea in the emergency department".) ●Exertional, positional, and nocturnal dyspnea – <span>Chronic exertional dyspnea and paroxysmal nocturnal dyspnea (PND) are both associated with heart failure, although nocturnal dyspnea is more specific to heart failure. Asthma is also associated with exertional and nocturnal dyspnea, but unlike PND does not usually improve with sitting or standing. Orthopnea, the development of or worsening of dyspnea in the supine position, is also associated with heart failure and increased pulmonary capillary pressure due to the increased venou




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Orthopnea, the development of or worsening of dyspnea in the supine position, is also associated with heart failure and increased pulmonary capillary pressure due to the increased venous return to the heart in this position. Central obesity, however, with a large protuberant abdomen, may also lead to orthopnea; increased intra-abdominal pressure associated with large abdominal girth impairs movement of the diaphragm during inhalation. Finally, patients with inspiratory muscle weakness may also complain of orthopnea due to the increased work of breathing associated with moving the diaphragm against high intra-abdominal pressure.
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although nocturnal dyspnea is more specific to heart failure. Asthma is also associated with exertional and nocturnal dyspnea, but unlike PND does not usually improve with sitting or standing. <span>Orthopnea, the development of or worsening of dyspnea in the supine position, is also associated with heart failure and increased pulmonary capillary pressure due to the increased venous return to the heart in this position. Central obesity, however, with a large protuberant abdomen, may also lead to orthopnea; increased intra-abdominal pressure associated with large abdominal girth impairs movement of the diaphragm during inhalation. Finally, patients with inspiratory muscle weakness may also complain of orthopnea due to the increased work of breathing associated with moving the diaphragm against high intra-abdominal pressure. Bendopnea, the worsening of dyspnea when leaning forward, is described in patients with decompensated heart failure [18]. Dyspnea that is not exacerbated by exertion is more often due t




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Bendopnea, the worsening of dyspnea when leaning forward, is described in patients with decompensated heart failure [18].
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ally, patients with inspiratory muscle weakness may also complain of orthopnea due to the increased work of breathing associated with moving the diaphragm against high intra-abdominal pressure. <span>Bendopnea, the worsening of dyspnea when leaning forward, is described in patients with decompensated heart failure [18]. Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease. ●Intermittent dyspnea – Intermittent dyspnea associa




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Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease.
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ciated with moving the diaphragm against high intra-abdominal pressure. Bendopnea, the worsening of dyspnea when leaning forward, is described in patients with decompensated heart failure [18]. <span>Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease. ●Intermittent dyspnea – Intermittent dyspnea associated with cold air or animal dander exposure suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea follow




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Intermittent dyspnea associated with cold air or animal dander exposure suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea following upper respiratory infections may be due to asthma or chronic obstructive pulmonary disease (COPD).
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th decompensated heart failure [18]. Dyspnea that is not exacerbated by exertion is more often due to a functional or perceptual problem than to cardiopulmonary disease. ●Intermittent dyspnea – <span>Intermittent dyspnea associated with cold air or animal dander exposure suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea following upper respiratory infections may be due to asthma or chronic obstructive pulmonary disease (COPD). In addition to asthma, intermittent symptoms that resolve completely between episodes can be seen with recurrent aspiration; recurrent pulmonary emboli and heart failure can also wax an




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In addition to asthma, intermittent symptoms that resolve completely between episodes can be seen with recurrent aspiration; recurrent pulmonary emboli and heart failure can also wax and wane, but generally are characterized by a baseline level of dysfunction. The presence of specific, reproducible inciting events such as exercise or cold air exposure is common with airways hyperreactivity.
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e suggests asthma; work-related dyspnea may suggest occupational asthma; and dyspnea following upper respiratory infections may be due to asthma or chronic obstructive pulmonary disease (COPD). <span>In addition to asthma, intermittent symptoms that resolve completely between episodes can be seen with recurrent aspiration; recurrent pulmonary emboli and heart failure can also wax and wane, but generally are characterized by a baseline level of dysfunction. The presence of specific, reproducible inciting events such as exercise or cold air exposure is common with airways hyperreactivity. ●Rapidity of symptom onset and progression – The rapidity with which symptoms develop during exercise can also provide useful diagnostic information. For example, patients who develop s




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The rapidity with which symptoms develop during exercise can also provide useful diagnostic information. For example, patients who develop shortness of breath and wheezing after walking 50 to 100 feet often have acute elevations in pulmonary capillary wedge pressure (usually due to cardiac diastolic dysfunction) or pulmonary hypertension. In contrast, symptoms of exercise-induced asthma usually are precipitated by more intense activity, beginning three minutes into exercise, peaking within 10 to 15 minutes, and resolving by 60 minutes.
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of dysfunction. The presence of specific, reproducible inciting events such as exercise or cold air exposure is common with airways hyperreactivity. ●Rapidity of symptom onset and progression – <span>The rapidity with which symptoms develop during exercise can also provide useful diagnostic information. For example, patients who develop shortness of breath and wheezing after walking 50 to 100 feet often have acute elevations in pulmonary capillary wedge pressure (usually due to cardiac diastolic dysfunction) or pulmonary hypertension. In contrast, symptoms of exercise-induced asthma usually are precipitated by more intense activity, beginning three minutes into exercise, peaking within 10 to 15 minutes, and resolving by 60 minutes. (See "Exercise-induced bronchoconstriction".) Respiratory muscle weakness generally leads to gradually progressive dyspnea, sometimes with an acute worsening at a time of illness, parti




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Respiratory muscle weakness generally leads to gradually progressive dyspnea, sometimes with an acute worsening at a time of illness, particularly a respiratory infection.
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lly are precipitated by more intense activity, beginning three minutes into exercise, peaking within 10 to 15 minutes, and resolving by 60 minutes. (See "Exercise-induced bronchoconstriction".) <span>Respiratory muscle weakness generally leads to gradually progressive dyspnea, sometimes with an acute worsening at a time of illness, particularly a respiratory infection. Severity of dyspnea — For patients with chronic dyspnea, formal assessment of the severity of dyspnea can help create a baseline for future comparisons [19]. A number of instruments are




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For patients with chronic dyspnea, formal assessment of the severity of dyspnea can help create a baseline for future comparisons [19]. A number of instruments are available to help assess the severity of dyspnea, such as the Baseline Dyspnea Index, the Modified Medical Research Council (mMRC) dyspnea scale (table 3), and the Borg scale (table 4) [20-24]. It is important to note that scales like the mMRC do not measure dyspnea directly; rather, they assess the intensity of exercise that provokes dyspnea and, indirectly, the degree of disability resulting from dyspnea.
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Respiratory muscle weakness generally leads to gradually progressive dyspnea, sometimes with an acute worsening at a time of illness, particularly a respiratory infection. Severity of dyspnea — <span>For patients with chronic dyspnea, formal assessment of the severity of dyspnea can help create a baseline for future comparisons [19]. A number of instruments are available to help assess the severity of dyspnea, such as the Baseline Dyspnea Index, the Modified Medical Research Council (mMRC) dyspnea scale (table 3), and the Borg scale (table 4) [20-24]. It is important to note that scales like the mMRC do not measure dyspnea directly; rather, they assess the intensity of exercise that provokes dyspnea and, indirectly, the degree of disability resulting from dyspnea. Associated symptoms — Associated symptoms such as cough, sputum production, nasal congestion, chest pain, peripheral edema, Raynaud phenomenon, joint swelling, and muscle weakness can h




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Attention to the quality or descriptor that a patient associates with the breathing discomfort often provides clues to the underlying diagnosis [25]. This observation comes from studies in which dyspnea questionnaires (table 5) were presented to patients with breathing discomfort from a variety of cardiopulmonary disorders [6-8,26].
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ith interstitial lung disease or pulmonary hypertension; and symmetric swelling of the metacarpophalangeal joints may be a clue to rheumatoid lung disease. Descriptors of breathing discomfort — <span>Attention to the quality or descriptor that a patient associates with the breathing discomfort often provides clues to the underlying diagnosis [25]. This observation comes from studies in which dyspnea questionnaires (table 5) were presented to patients with breathing discomfort from a variety of cardiopulmonary disorders [6-8,26]. Subjects were asked to select the phrases that best described their breathing discomfort, and distinct clusters emerged. While some clusters of phrases were common to a number of diseas




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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.
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eathing discomfort from a variety of cardiopulmonary disorders [6-8,26]. Subjects were asked to select the phrases that best described their breathing discomfort, and distinct clusters emerged. <span>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. The combined data from studies that were performed in patients with known cardiopulmonary disorders or in normal subjects made breathless under experimental conditions indicate the foll




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The sensation of "air hunger" has been associated with acute bronchoconstriction and hyperinflation in asthma and COPD, heart failure, pulmonary embolism, and restricted thoracic motion, as well as acute hypercapnia from any cause [3,4,27].
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studies that were performed in patients with known cardiopulmonary disorders or in normal subjects made breathless under experimental conditions indicate the following (table 6) [2,6-8,25,26]: ●<span>The sensation of "air hunger" has been associated with acute bronchoconstriction and hyperinflation in asthma and COPD, heart failure, pulmonary embolism, and restricted thoracic motion, as well as acute hypercapnia from any cause [3,4,27]. ●Acute bronchoconstriction leads to a series of sensations as the degree of obstruction worsens, from "chest tightness" to an increased "effort to breathe" to a sensation of "air hunger




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Acute bronchoconstriction leads to a series of sensations as the degree of obstruction worsens, from "chest tightness" to an increased "effort to breathe" to a sensation of "air hunger" [6-9,12,13]. The sensation of "tightness" appears to be independent of the work of breathing [28]. Attention to the use of verbal descriptors of dyspnea may help the clinician avoid underestimation of the severity of airflow limitation when objective measurements of lung function are not possible.
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d with acute bronchoconstriction and hyperinflation in asthma and COPD, heart failure, pulmonary embolism, and restricted thoracic motion, as well as acute hypercapnia from any cause [3,4,27]. ●<span>Acute bronchoconstriction leads to a series of sensations as the degree of obstruction worsens, from "chest tightness" to an increased "effort to breathe" to a sensation of "air hunger" [6-9,12,13]. The sensation of "tightness" appears to be independent of the work of breathing [28]. Attention to the use of verbal descriptors of dyspnea may help the clinician avoid underestimation of the severity of airflow limitation when objective measurements of lung function are not possible. ●Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis. ●Patients with COPD and dynamic hyperinflation sometimes c




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Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis.
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on to the use of verbal descriptors of dyspnea may help the clinician avoid underestimation of the severity of airflow limitation when objective measurements of lung function are not possible. ●<span>Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis. ●Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. ●A sensation of rapid, sh




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Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9].
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on when objective measurements of lung function are not possible. ●Report of "increased work of breathing" is associated with COPD, moderate to severe asthma, myopathy, and pulmonary fibrosis. ●<span>Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. ●A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance. ●Heart failure is also associated with a sensation of "suffocation




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● A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance.

● Heart failure is also associated with a sensation of "suffocation" [6].

● A sense of heavy breathing is typical of deconditioning.

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myopathy, and pulmonary fibrosis. ●Patients with COPD and dynamic hyperinflation sometimes complain of a sensation of "unsatisfying breaths" or a sense that they "cannot get a deep breath" [9]. <span>●A sensation of rapid, shallow breathing may correspond to interstitial lung disease or reduced chest wall compliance. ●Heart failure is also associated with a sensation of "suffocation" [6]. ●A sense of heavy breathing is typical of deconditioning. Patient questionnaires have been developed for use in research and clinical settings, and allow the doctor to assess symptom intensity, quality, and associated affective responses as pa




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The absence of cigarette smoking argues strongly against a diagnosis of COPD, unless the patient has a history of tuberculosis or use of biomass cooking fuels. In one study, a history of smoking cigarettes had a positive predictive value for COPD of 0.4; COPD is uncommon among patients who have never smoked or have smoked less than 10 pack years [37].
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the wording used to describe dyspnea [31-36]. Further research in this area is underway. (See 'Perceptual and psychological factors' below.) Cigarette smoking and exposures to dusts and fumes — <span>The absence of cigarette smoking argues strongly against a diagnosis of COPD, unless the patient has a history of tuberculosis or use of biomass cooking fuels. In one study, a history of smoking cigarettes had a positive predictive value for COPD of 0.4; COPD is uncommon among patients who have never smoked or have smoked less than 10 pack years [37]. The occupational history may lead to diagnosis of diseases such as asbestosis, chronic beryllium disease, silicosis, or another pneumoconiosis. (See "Asbestos-related pleuropulmonary di




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A complete physical examination is essential. In particular, attention should be directed at the presence or absence of stridor, wheezing, crackles, tachycardia, arrhythmia, heart murmurs, gallop, peripheral edema, muscle weakness, dysphonia, and evidence of rheumatic disease. However, the absence of physical findings tends to have a greater negative predictive value, than the positive predictive value of any identified signs [17].
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c beryllium disease, silicosis, or another pneumoconiosis. (See "Asbestos-related pleuropulmonary disease" and "Chronic beryllium disease (berylliosis)" and "Silicosis".) Physical examination — <span>A complete physical examination is essential. In particular, attention should be directed at the presence or absence of stridor, wheezing, crackles, tachycardia, arrhythmia, heart murmurs, gallop, peripheral edema, muscle weakness, dysphonia, and evidence of rheumatic disease. However, the absence of physical findings tends to have a greater negative predictive value, than the positive predictive value of any identified signs [17]. ●Clubbing is associated with a number of causes of dyspnea, including bronchiectasis, idiopathic pulmonary fibrosis, lung cancer, and cyanotic heart disease, but not asthma or COPD. ●Ju




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Abdominal rounding, the protruding of the central abdomen with diminished transverse diameter during exhalation, has been associated with acute heart failure [38].
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n may suggest left sided heart failure or cor pulmonale. ●Decreased or distant heart sounds may suggest a pericardial effusion, but may also be due to obesity or hyperinflation from emphysema. ●<span>Abdominal rounding, the protruding of the central abdomen with diminished transverse diameter during exhalation, has been associated with acute heart failure [38]. EVALUATION OF ACUTE DYSPNEA — Breathing discomfort arising over the course of minutes to hours is generally due to a limited number of conditions (table 2) and generally involves proces




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Clues to the need for an urgent evaluation include heart rate >120 beats/minute, respiratory rate >30 breaths/minute, pulse oxygen saturation (SpO2) <90 percent, use of accessory respiratory muscles, difficulty speaking in full sentences, stridor, asymmetric breath sounds or percussion, diffuse crackles, diaphoresis, and cyanosis
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iscomfort arising over the course of minutes to hours is generally due to a limited number of conditions (table 2) and generally involves processes that require prompt evaluation and treatment. <span>Clues to the need for an urgent evaluation include heart rate >120 beats/minute, respiratory rate >30 breaths/minute, pulse oxygen saturation (SpO2) <90 percent, use of accessory respiratory muscles, difficulty speaking in full sentences, stridor, asymmetric breath sounds or percussion, diffuse crackles, diaphoresis, and cyanosis. The evaluation of dyspnea in the emergency department is described separately. (See "Evaluation of the adult with dyspnea in the emergency department".) INITIAL TESTING IN CHRONIC DYSP




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The majority of patients with chronic dyspnea of unclear etiology have one of five diagnoses, although the spectrum of potential causes is broad and more than one etiology may be present (table 7) [17,37,39].
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e diagnostic approach of initial testing, follow-up testing, and advanced testing, starting with the tests that are the least invasive and most likely to yield a diagnosis. Most common causes — <span>The majority of patients with chronic dyspnea of unclear etiology have one of five diagnoses, although the spectrum of potential causes is broad and more than one etiology may be present (table 7) [17,37,39]. It is also important to remember that the presence of a known chronic cardiopulmonary disease does not guarantee that the patient's symptoms or the etiology of their exercise limitation




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The five most common causes of chronic dyspnea are the following:

● Asthma (see 'Respiratory' above)

● Chronic obstructive pulmonary disease (COPD) (see 'Respiratory' above)

● Interstitial lung disease (see 'Respiratory' above)

● Myocardial dysfunction (see 'Cardiovascular' above)

● Obesity/deconditioning (see 'Cardiovascular' above)

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ulmonary disease does not guarantee that the patient's symptoms or the etiology of their exercise limitation are due to that condition, particularly in patients with coexisting conditions [16]. <span>The five most common causes of chronic dyspnea are the following: ●Asthma (see 'Respiratory' above) ●Chronic obstructive pulmonary disease (COPD) (see 'Respiratory' above) ●Interstitial lung disease (see 'Respiratory' above) ●Myocardial dysfunction (see 'Cardiovascular' above) ●Obesity/deconditioning (see 'Cardiovascular' above) Pace of testing — For patients with chronic dyspnea, the severity of dyspnea and rate of worsening are important determinants of the pace and location of diagnostic testing [19]. The op




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The optimal sequence of diagnostic testing for chronic dyspnea has not been determined. We typically follow an algorithm that utilizes three tiers of testing: initial testing (table 8), follow-up testing based on results of initial tests (table 9A and table 9B and table 9C), and advanced testing if the diagnosis remains uncertain (table 10).
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scular' above) Pace of testing — For patients with chronic dyspnea, the severity of dyspnea and rate of worsening are important determinants of the pace and location of diagnostic testing [19]. <span>The optimal sequence of diagnostic testing for chronic dyspnea has not been determined. We typically follow an algorithm that utilizes three tiers of testing: initial testing (table 8), follow-up testing based on results of initial tests (table 9A and table 9B and table 9C), and advanced testing if the diagnosis remains uncertain (table 10). Within each tier, we select tests based on the patient’s clinical features, results of prior tests, and likelihood of a diagnostic result. One study found that the most informative test




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One study found that the most informative tests for adults (age 45 to 84) with dyspnea and no known cardiopulmonary disease were the forced expiratory volume in one second (FEV1) obtained by spirometry, the N-terminal pro-brain natriuretic peptide (NT-proBNP), and percent emphysema on chest computed tomography [40].
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testing if the diagnosis remains uncertain (table 10). Within each tier, we select tests based on the patient’s clinical features, results of prior tests, and likelihood of a diagnostic result. <span>One study found that the most informative tests for adults (age 45 to 84) with dyspnea and no known cardiopulmonary disease were the forced expiratory volume in one second (FEV1) obtained by spirometry, the N-terminal pro-brain natriuretic peptide (NT-proBNP), and percent emphysema on chest computed tomography [40]. Specific tests — After reviewing the clinical findings for patterns that appear suggestive of one or two of the above five most common processes, the narrowed differential diagnosis is




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If the clinical evaluation doesn’t allow narrowing of the differential we usually obtain the following "initial tests" (table 8):

● Complete blood count (to exclude anemia): The degree of dyspnea associated with anemia may depend on the rapidity of blood loss and the degree of exertion that the patient undertakes. (See 'Cardiovascular' above.)

● Glucose, blood urea nitrogen, creatinine, electrolytes.

● Thyroid stimulating hormone (TSH).

● Spirometry pre and post inhaled bronchodilator OR full pulmonary function tests (PFTs) if the clinical evaluation does not suggest asthma or COPD.

● Pulse oximetry during ambulation at a normal pace over approximately 200 meters and/or up two to three flights of stairs.

● Chest radiograph.

● Electrocardiogram.

● Plasma BNP or NT-pro BNP

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ary artery disease, peripheral edema, and no smoking history might be evaluated for heart failure with an electrocardiogram, a serum NT-proBNP, and echocardiogram before considering spirometry. <span>If the clinical evaluation doesn’t allow narrowing of the differential we usually obtain the following "initial tests" (table 8): ●Complete blood count (to exclude anemia): The degree of dyspnea associated with anemia may depend on the rapidity of blood loss and the degree of exertion that the patient undertakes. (See 'Cardiovascular' above.) ●Glucose, blood urea nitrogen, creatinine, electrolytes. ●Thyroid stimulating hormone (TSH). ●Spirometry pre and post inhaled bronchodilator OR full pulmonary function tests (PFTs) if the clinical evaluation does not suggest asthma or COPD. ●Pulse oximetry during ambulation at a normal pace over approximately 200 meters and/or up two to three flights of stairs. ●Chest radiograph. ●Electrocardiogram. ●Plasma BNP or NT-pro BNP Spirometry can identify the presence and severity of airflow obstruction, and when both FEV1 and forced vital capacity (FVC) are reduced proportionately (ie, the FEV1/FVC ratio is norma




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Typically in asthma, airflow limitation is reversible, although a large component of airways edema and inflammation may need a course of inhaled or oral glucocorticoid therapy to achieve complete reversibility
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gested. When intrathoracic airflow limitation is noted or when a diagnosis of asthma is suspected, postbronchodilator spirometry determines whether there is reversibility of airflow limitation. <span>Typically in asthma, airflow limitation is reversible, although a large component of airways edema and inflammation may need a course of inhaled or oral glucocorticoid therapy to achieve complete reversibility. Patients with a clinical suspicion of asthma and reversible airflow limitation on spirometry would be managed with a trial of specific therapy for asthma. Patients with a smoking histo




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Patients with a smoking history longer than 20 years and irreversible airflow limitation on spirometry are usually managed with a presumptive diagnosis of chronic obstructive pulmonary disease (COPD). However, other causes of irreversible airflow limitation (eg, bronchiectasis, bronchiolitis, central airway obstruction) should be considered if the patient does not respond to empiric therapy for asthma or COPD
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apy to achieve complete reversibility. Patients with a clinical suspicion of asthma and reversible airflow limitation on spirometry would be managed with a trial of specific therapy for asthma. <span>Patients with a smoking history longer than 20 years and irreversible airflow limitation on spirometry are usually managed with a presumptive diagnosis of chronic obstructive pulmonary disease (COPD). However, other causes of irreversible airflow limitation (eg, bronchiectasis, bronchiolitis, central airway obstruction) should be considered if the patient does not respond to empiric therapy for asthma or COPD. (See "Asthma in adolescents and adults: Evaluation and diagnosis", section on 'Diagnosis' and "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, an




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The second phase of the evaluation of dyspnea is aimed at clarifying abnormalities that were noted on initial testing, but were not diagnostic (table 9A and table 9C and table 9B)
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diseases and restrictive physiology", section on 'Kyphosis and scoliosis' and "Determining the etiology and severity of heart failure or cardiomyopathy".) FOLLOW-UP TESTING IN CHRONIC DYSPNEA — <span>The second phase of the evaluation of dyspnea is aimed at clarifying abnormalities that were noted on initial testing, but were not diagnostic (table 9A and table 9C and table 9B). In addition, some patients will have had normal results on initial testing, but have persistent symptoms that require further evaluation. Pulmonary function tests — Patients with findi




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A restrictive pattern may be caused by interstitial lung disease, pleural disease (eg, trapped lung), chest wall disease (eg, kyphoscoliosis), or ventilatory muscle weakness (eg, diffuse or due to diaphragmatic paralysis). Respiratory muscle weakness can be evaluated further with maximal inspiratory and expiratory pressures at the mouth, maximal voluntary ventilation in one minute, and supine spirometry that is compared with sitting spirometry results
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The possibility of an underlying "restrictive" abnormality is assessed with measurement of lung volumes, looking for a similar decrease in total lung capacity and functional residual capacity. <span>A restrictive pattern may be caused by interstitial lung disease, pleural disease (eg, trapped lung), chest wall disease (eg, kyphoscoliosis), or ventilatory muscle weakness (eg, diffuse or due to diaphragmatic paralysis). Respiratory muscle weakness can be evaluated further with maximal inspiratory and expiratory pressures at the mouth, maximal voluntary ventilation in one minute, and supine spirometry that is compared with sitting spirometry results. (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Diagnostic evaluation' and "Tests of respiratory muscle strength".)




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Alternatively, if total lung capacity and residual volume are normal or increased, the decrease in vital capacity may be an indicator of reduced elastic recoil or air trapping and the patient may have emphysema or bronchiolitis without airflow limitation that is measurable on spirometry
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results. (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation", section on 'Diagnostic evaluation' and "Tests of respiratory muscle strength".) <span>Alternatively, if total lung capacity and residual volume are normal or increased, the decrease in vital capacity may be an indicator of reduced elastic recoil or air trapping and the patient may have emphysema or bronchiolitis without airflow limitation that is measurable on spirometry. (See "Office spirometry" and "Pulmonary function testing in asthma".) ●Suspicion for asthma with normal baseline spirometry – Bronchoprovocation testing (eg, with methacholine, histami




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Bronchoprovocation testing (eg, with methacholine, histamine, or mannitol) is typically obtained in patients with recurrent, episodic dyspnea suggestive of asthma who have normal or near normal spirometry. A trial of therapy for asthma is an alternative, but bronchoprovocation is preferred to enable a precise determination of asthma. Studies have shown that up to 30 percent of patients with a clinical diagnosis of asthma do not have airway reactivity on formal testing [41,42].
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olitis without airflow limitation that is measurable on spirometry. (See "Office spirometry" and "Pulmonary function testing in asthma".) ●Suspicion for asthma with normal baseline spirometry – <span>Bronchoprovocation testing (eg, with methacholine, histamine, or mannitol) is typically obtained in patients with recurrent, episodic dyspnea suggestive of asthma who have normal or near normal spirometry. A trial of therapy for asthma is an alternative, but bronchoprovocation is preferred to enable a precise determination of asthma. Studies have shown that up to 30 percent of patients with a clinical diagnosis of asthma do not have airway reactivity on formal testing [41,42]. Empiric therapy can lead to gradual acceleration of treatment, including use of systemic glucocorticoids, with attendant side effects if the patient does not have asthma. (See "Bronchop




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Pulmonary vascular disease (eg, pulmonary hypertension, chronic thromboembolic disease, pulmonary veno-occlusive disease) is suggested by the combination of normal spirometry and lung volumes, but abnormal gas transfer manifest by a decrease in DLCO and pulse oxygen saturation on exertion (eg, ≥5 percent).
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cularly in the identification of interstitial lung disease (suggested by reduced lung volumes), emphysema or bronchiolitis (suggested by an obstructive pattern), and pulmonary vascular disease. <span>Pulmonary vascular disease (eg, pulmonary hypertension, chronic thromboembolic disease, pulmonary veno-occlusive disease) is suggested by the combination of normal spirometry and lung volumes, but abnormal gas transfer manifest by a decrease in DLCO and pulse oxygen saturation on exertion (eg, ≥5 percent). (See "Diffusing capacity for carbon monoxide".) ●Low oxygen saturation – A low resting oxygen saturation (eg, ≤95 percent) or a significant decline in oxygen saturation during exercise




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A low resting oxygen saturation (eg, ≤95 percent) or a significant decline in oxygen saturation during exercise (≥5 percent) warrants further evaluation. The differential diagnosis includes COPD, interstitial lung disease, pulmonary vascular disease, bronchiolitis obliterans, intrapulmonary or intracardiac shunt, and heart failure. Thus, such patients typically need high resolution computed tomography (HRCT) and a transthoracic echocardiogram, possibly with a bubble study
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umes, but abnormal gas transfer manifest by a decrease in DLCO and pulse oxygen saturation on exertion (eg, ≥5 percent). (See "Diffusing capacity for carbon monoxide".) ●Low oxygen saturation – <span>A low resting oxygen saturation (eg, ≤95 percent) or a significant decline in oxygen saturation during exercise (≥5 percent) warrants further evaluation. The differential diagnosis includes COPD, interstitial lung disease, pulmonary vascular disease, bronchiolitis obliterans, intrapulmonary or intracardiac shunt, and heart failure. Thus, such patients typically need high resolution computed tomography (HRCT) and a transthoracic echocardiogram, possibly with a bubble study. ●Reduced lung volumes and obesity – Obesity is associated with reductions in expiratory reserve volume and function residual capacity and, in some patients, a decrease in total lung ca




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Obesity is associated with reductions in expiratory reserve volume and function residual capacity and, in some patients, a decrease in total lung capacity (restrictive ventilatory defect) [43]. However, the changes in lung volumes do not necessarily correlate with dyspnea and it can be difficult to know whether this pattern of reduced lung volumes is due to obesity or another respiratory disease. In a population study (NHANES III), subjects in the highest quintile of body mass index (BMI), had the lowest risk for significant airflow obstruction, so obesity by itself is less commonly a cause of classical airflow obstruction [44].
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eart failure. Thus, such patients typically need high resolution computed tomography (HRCT) and a transthoracic echocardiogram, possibly with a bubble study. ●Reduced lung volumes and obesity – <span>Obesity is associated with reductions in expiratory reserve volume and function residual capacity and, in some patients, a decrease in total lung capacity (restrictive ventilatory defect) [43]. However, the changes in lung volumes do not necessarily correlate with dyspnea and it can be difficult to know whether this pattern of reduced lung volumes is due to obesity or another respiratory disease. In a population study (NHANES III), subjects in the highest quintile of body mass index (BMI), had the lowest risk for significant airflow obstruction, so obesity by itself is less commonly a cause of classical airflow obstruction [44]. (See "Chest wall diseases and restrictive physiology", section on 'Obesity'.) Chest computed tomography — Chest computed tomography (CT) is helpful in the evaluation of dyspnea in the f




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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.
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graphy — Chest computed tomography (CT) is helpful in the evaluation of dyspnea in the following settings (table 9B): ●Abnormalities on the chest radiograph that need further characterization – <span>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. ●When HRCT is helpful despite a normal chest radiograph – A small percentage of patients with interstitial lung disease may have a normal chest radiograph on presentation; HRCT scan cle




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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
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e are best evaluated by measurement of a serum N-terminal pro-brain natriuretic peptide (NT-pro BNP) or transthoracic echocardiography. ●When HRCT is helpful despite a normal chest radiograph – <span>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. (See "High resolution computed tomography of the lungs".) A minority of patients with a history of cigarette smoking, normal spirometry, and normal chest radiographs have extensive emp




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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.
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confirm HF due to reduced left ventricular (LV) systolic function (HF-REF). (See "Determining the etiology and severity of heart failure or cardiomyopathy".) ●Suspected diastolic dysfunction – <span>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. Additional Doppler features of diastolic dysfunction include elevated pulmonary artery systolic pressure, and impaired ventricular relaxation (eg, early/late [E/A] filling <1). HF-PE




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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.
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jection fraction: Clinical manifestations and diagnosis", section on 'Echocardiography' and "Treatment and prognosis of heart failure with preserved ejection fraction", section on 'Treatment'.) <span>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. ●Suspected pericardial disease – Constrictive pericarditis can be difficult to diagnose in patients who present with chronic dyspnea, although patients generally have peripheral edema.




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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
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n tests, and a chest radiograph), nearly two-thirds have evidence of diastolic dysfunction [48], which can manifest as dyspnea with relatively minimal exertion. ●Suspected pericardial disease – <span>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. (See "Constrictive pericarditis", section on 'Two-dimensional and M-mode' and "Variants of constrictive pericarditis".) ●Suspected pulmonary hypertension – Elevated pulmonary artery (P




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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)
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o the adult with interstitial lung disease: Diagnostic testing" and "Interpretation of lung biopsy results in interstitial lung disease".) Pulmonary hypertension suggested by echocardiography — <span>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). The evaluation of pulmonary hypertension is described separately. (See "Echocardiographic evaluation of the pulmonic valve and pulmonary artery", section on 'Pulmonary hemodynamics' an




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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.
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production and oxygen uptake), and relationship of minute ventilation to carbon dioxide production. (See "Cardiopulmonary exercise testing in cardiovascular disease" and "Exercise physiology".) <span>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. (See "Mitochondrial myopathies: Clinical features and diagnosis", section on 'Exercise testing'.) A CPET may be helpful in providing support for the presence of deconditioning or in det




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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.
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en extraction (increased mixed venous oxygen), and an increase in blood lactate after exercise. (See "Mitochondrial myopathies: Clinical features and diagnosis", section on 'Exercise testing'.) <span>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. In patients with both pulmonary and cardiac disease, either of which could cause the patient to have dyspnea limiting their exercise capacity, CPET may assist in the determination of th




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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.
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st consistent with deconditioning or obesity. While obese patients frequently report dyspnea [52], in a given individual it can be difficult to know how much dyspnea is attributable to obesity. <span>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. The re-evaluation is important due to the infrequent situation in which a treatable cause of dyspnea is missed initially, but becomes apparent on subsequent testing. Dyspnea due to obes




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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.
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s the sense of respiratory work or effort [54]. The context in which a sensation occurs may alter the affective component of the intensity and needs to be considered when assessing the patient. <span>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. To the extent that dyspnea occurs unexpectedly or cannot be quickly relieved, it may give rise to a range of emotional reactions, which can then lead to further physiological derangemen




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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".)
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ffective response may contribute to the intensity or discomfort of the sensation [54]; questionnaires have been developed that incorporate both qualitative and affective descriptors [29,30,54]. <span>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".) Sex, ethnicity, and cultural context appear to influence an individual's description of dyspnea, but further research is needed to understand the exact differences and their effects on




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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.

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es 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. <span>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 disordered or inadequate breathing. This topic review will provide a differential diagnosis of the life-t




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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]
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separately. (See "Physiology of dyspnea" and "Measures of oxygenation and mechanisms of hypoxemia".) EPIDEMIOLOGY — Dyspnea is a common chief complaint among emergency department (ED) patients. <span>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]. In males and females over the age of 65 years old, dyspnea and related problems were a major reason for ED visits [3]. Epidemiologically, the most common diagnoses among older adult pa




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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]
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chief complaints (eg, cough, chest discomfort) comprised 8.8 percent [2]. In males and females over the age of 65 years old, dyspnea and related problems were a major reason for ED visits [3]. <span>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]. DIFFERENTIAL DIAGNOSIS — A table listing life-threatening and common causes of dyspnea that present to the emergency department (ED) is provided (table 1). Life-threatening upper airwa




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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
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DIFFERENTIAL DIAGNOSIS — A table listing life-threatening and common causes of dyspnea that present to the emergency department (ED) is provided (table 1). Life-threatening upper airway causes ●<span>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. (See "Airway foreign bodies in adults".) ●Angioedema – Angioedema can cause significant swelling of the lips, tongue, posterior pharynx, and most dangerously the larynx; this can occur




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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].
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uth 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. (See "Airway foreign bodies in adults".) ●Angioedema – <span>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]. (See "Hereditary angioedema: Acute treatment of angioedema attacks" and "An overview of angioedema: Pathogenesis and causes".) ●Anaphylaxis – Often triggered by foods, insect bites, and




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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).
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be hemilingual and contralateral to the ischemic hemisphere [5]. (See "Hereditary angioedema: Acute treatment of angioedema attacks" and "An overview of angioedema: Pathogenesis and causes".) ●<span>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). (See "Anaphylaxis: Emergency treatment".) ●Infections of the pharynx and neck – A number of oropharyngeal infections can cause acute dyspnea [6-9]. Epiglottitis generally presents with




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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.
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xia), cardiovascular compromise (eg, hypotension, tachycardia, syncope), and gastrointestinal complaints (eg, abdominal pain, vomiting, and diarrhea). (See "Anaphylaxis: Emergency treatment".) ●<span>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. (See "Epiglottitis (supraglottitis): Clinical features and diagnosis" and "Pertussis infection in adolescents and adults: Clinical manifestations and diagnosis" and "Deep neck space inf




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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.
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titis (supraglottitis): Clinical features and diagnosis" and "Pertussis infection in adolescents and adults: Clinical manifestations and diagnosis" and "Deep neck space infections in adults".) ●<span>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. (See "Penetrating neck injuries: Initial evaluation and management" and "Emergency care of moderate and severe thermal burns in adults" and "Inhalation injury from heat, smoke, or chemi




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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.
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aluation and management" and "Emergency care of moderate and severe thermal burns in adults" and "Inhalation injury from heat, smoke, or chemical irritants".) Life-threatening pulmonary causes ●<span>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. (See "Overview of acute pulmonary embolism in adults" and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Fat em




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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
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osis of the nonpregnant adult with suspected acute pulmonary embolism" and "Fat embolism syndrome" and "Acute chest syndrome in adults with sickle cell disease" and "Amniotic fluid embolism".) ●<span>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. (See "COPD exacerbations: Management".) ●Asthma – Asthma exacerbations generally present with dyspnea and wheezing. Signs of severe disease include the use of accessory muscles, brief




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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.
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esponsible for up to 25 percent of apparent "COPD exacerbations" and should be suspected when the patient fails to improve with standard COPD treatment. (See "COPD exacerbations: Management".) ●<span>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. (See "Acute exacerbations of asthma in adults: Home and office management" and "Emergency airway management in acute severe asthma".) ●Pneumothorax and pneumomediastinum – Any simple pn




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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. (
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pressed mental status portend imminent respiratory arrest. (See "Acute exacerbations of asthma in adults: Home and office management" and "Emergency airway management in acute severe asthma".) ●<span>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. (See "Initial evaluation and management of blunt thoracic trauma in adults".) Risk factors for primary spontaneous pneumothorax include smoking, a family history, and Marfan syndrome. Pat




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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".)

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ement, intubation, and barotrauma), a number of medical conditions increase the risk for developing a pneumothorax. (See "Initial evaluation and management of blunt thoracic trauma in adults".) <span>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




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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.
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tic fibrosis, tuberculosis, and AIDS patients with pneumocystis pneumonia) are at risk for secondary spontaneous pneumothorax. (See "Treatment of secondary spontaneous pneumothorax in adults".) <span>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




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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.
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mothorax and present with dyspnea, sharp pleuritic chest pain, and subcutaneous emphysema over the supraclavicular area and anterior neck from pneumomediastinum associated with a pneumothorax. ●<span>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. (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".) Pneumonia and other manifestations of infection with coronavirus disease 2019 (COVID-19) a




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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).
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disease 2019 (COVID-19) are discussed in a number of UpToDate topics. (See "COVID-19: Clinical features" and "COVID-19: Diagnosis" and "COVID-19: Critical care and airway management issues".) ●<span>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). (See "Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults" and "Acute respiratory distress syndrome: Clinical features, diagnosis, and




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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.
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tory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults" and "Acute respiratory distress syndrome: Clinical features, diagnosis, and complications in adults".) ●<span>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. (See "High altitude pulmonary edema" and "Acute mountain sickness and high altitude cerebral edema".) ●Direct pulmonary injury – A pulmonary contusion or laceration is a possible source




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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.
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aluation and management of blunt thoracic trauma in adults".) ●Pulmonary hemorrhage – Hemorrhage from an injury or an underlying disease (eg, malignancy, tuberculosis) can cause acute dyspnea. ●<span>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. (See "E-cigarette or vaping product use associated lung injury (EVALI)".) Life-threatening cardiac causes ●Acute coronary syndrome (ACS) – Patients, particularly older adults, suffering




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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
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ntestinal complaints; and diffuse hazy or consolidative opacities on plain radiograph. (See "E-cigarette or vaping product use associated lung injury (EVALI)".) Life-threatening cardiac causes ●<span>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. (See "Diagnosis of acute myocardial infarction".) ●Acute decompensated heart failure (ADHF) – Symptomatic ADHF can be caused by volume overload, heart failure with preserved ejection f




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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.
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spnea as their sole symptom. Clinicians are more likely to miss an MI in the patient whose chief complaint is dyspnea, rather than chest pain. (See "Diagnosis of acute myocardial infarction".) ●<span>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. (See "Approach to diagnosis and evaluation of acute decompensated heart failure in adults".) ●Flash pulmonary edema – The sudden onset and rapid progression of pulmonary edema can be ca




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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.
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ated heart failure in adults".) ●Flash pulmonary edema – The sudden onset and rapid progression of pulmonary edema can be caused by ischemia, arrhythmia, hypertensive crisis, or drug overdose. ●<span>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. (See "Causes and pathophysiology of high-output heart failure".) ●Cardiomyopathy – The physiologic derangements associated with cardiomyopathy (primarily dilated cardiomyopathy) may res




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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).
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s hum heard over the internal jugular veins, and carotid bruits. An elevated troponin may be seen secondary to demand ischemia. (See "Causes and pathophysiology of high-output heart failure".) ●<span>Cardiomyopathy – The physiologic derangements associated with cardiomyopathy (primarily dilated cardiomyopathy) may result in pulmonary edema and manifest as dyspnea. Potential causes include cardiac ischemia, hypertension, alcohol abuse, cocaine abuse, and a number of systemic diseases (eg, sarcoidosis, systemic lupus erythematosus). (See "Causes of dilated cardiomyopathy".) ●Cardiac arrhythmia – Cardiac rhythm abnormalities, such as atrial flutter, atrial fibrillation, second- and third-degree heart block, and tach




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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.
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clude cardiac ischemia, hypertension, alcohol abuse, cocaine abuse, and a number of systemic diseases (eg, sarcoidosis, systemic lupus erythematosus). (See "Causes of dilated cardiomyopathy".) ●<span>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. (See "Overview of atrial fibrillation" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Approach to the diag




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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.
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See "Overview of atrial fibrillation" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Approach to the diagnosis".) ●<span>Valvular dysfunction – Aortic stenosis, mitral regurgitation, or ruptured chordae tendinae can present with acute dyspnea. A murmur may be appreciable, but the absence of an audible murmur does not exclude the diagnosis. (See "Valvular heart disease in elderly adults".) ●Cardiac tamponade – Whether due to trauma, malignancy, uremia, drugs, or infection, cardiac tamponade can present with acute dyspnea.




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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.
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dae tendinae can present with acute dyspnea. A murmur may be appreciable, but the absence of an audible murmur does not exclude the diagnosis. (See "Valvular heart disease in elderly adults".) ●<span>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. (See "Cardiac tamponade".) Life-threatening neurologic causes ●Stroke – Although dyspnea is not the chief complaint of patients with an acute stroke, a number of respiratory abnormaliti




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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.
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ent. The electrocardiogram (ECG) generally shows sinus tachycardia and low voltage and may uncommonly reveal electrical alternans. (See "Cardiac tamponade".) Life-threatening neurologic causes ●<span>Stroke – Although dyspnea is not the chief complaint of patients with an acute stroke, a number of respiratory abnormalities may result from a sufficiently severe injury or one affecting regions involved in respiration. Such abnormalities may include aspiration pneumonia, neurogenic pulmonary edema, and a number of abnormal respiratory patterns, including apnea, that can lead to severe hypoxia or hypocapnia. Invasive airway management may be required. (See "Complications of stroke: An overview", section on 'Pulmonary complications'.) ●Neuromuscular disease – A number of neuromuscular diseases, including multiple sclerosis, Guillain-B




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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.
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including apnea, that can lead to severe hypoxia or hypocapnia. Invasive airway management may be required. (See "Complications of stroke: An overview", section on 'Pulmonary complications'.) ●<span>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. (See "Manifestations of multiple sclerosis in adults" and "Guillain-Barré syndrome in adults: Clinical features and diagnosis" and "Clinical manifestations of myasthenia gravis" and "Cl




#Anemia #Anemie #Anémie #Diagnostique #Strategie #U2D
A number of specific causes of anemia diagnoses occur at increased frequency in individuals with malnutrition and/or malabsorption. These may include deficiencies of iron, vitamin B12, folate, and copper, which may occur in isolation or simultaneously. In individuals with severely reduced intake due to anorexia nervosa or starvation, the bone marrow is often affected.
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sion in older individuals with normocytic anemia and an unrevealing workup. The diagnosis should be reassessed periodically to avoid missing a correctable disorder. Malabsorption/malnutrition — <span>A number of specific causes of anemia diagnoses occur at increased frequency in individuals with malnutrition and/or malabsorption. These may include deficiencies of iron, vitamin B12, folate, and copper, which may occur in isolation or simultaneously. In individuals with severely reduced intake due to anorexia nervosa or starvation, the bone marrow is often affected. ●Gastric surgery – Gastric surgery, particularly bariatric surgery, is associated with malabsorption of vitamins and trace elements. This is particularly the case following Roux-en-Y pr




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Gastric surgery – Gastric surgery, particularly bariatric surgery, is associated with malabsorption of vitamins and trace elements. This is particularly the case following Roux-en-Y procedures [32]. Rates of deficiencies with different procedures and details of routine supplementation are discussed separately. (See "Bariatric surgery: Postoperative nutritional management".)

Zinc supplements – Zinc ingestion, as a dietary supplement or in zinc-containing denture adhesives, can cause copper deficiency by inhibiting copper absorption. (See "Causes and pathophysiology of the sideroblastic anemias", section on 'Copper deficiency'.)

Starvation or anorexia nervosa – Anemia is seen in approximately one-third of individuals with severe malnutrition or anorexia nervosa, either alone or in combination with neutropenia or leukopenia [33]. The bone marrow may show gelatinous necrosis. Anemia will improve with restored food intake.

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in B12, folate, and copper, which may occur in isolation or simultaneously. In individuals with severely reduced intake due to anorexia nervosa or starvation, the bone marrow is often affected. <span>●Gastric surgery – Gastric surgery, particularly bariatric surgery, is associated with malabsorption of vitamins and trace elements. This is particularly the case following Roux-en-Y procedures [32]. Rates of deficiencies with different procedures and details of routine supplementation are discussed separately. (See "Bariatric surgery: Postoperative nutritional management".) ●Zinc supplements – Zinc ingestion, as a dietary supplement or in zinc-containing denture adhesives, can cause copper deficiency by inhibiting copper absorption. (See "Causes and pathophysiology of the sideroblastic anemias", section on 'Copper deficiency'.) ●Starvation or anorexia nervosa – Anemia is seen in approximately one-third of individuals with severe malnutrition or anorexia nervosa, either alone or in combination with neutropenia or leukopenia [33]. The bone marrow may show gelatinous necrosis. Anemia will improve with restored food intake. (See "Anorexia nervosa in adults and adolescents: Medical complications and their management", section on 'Hematologic'.) Iron deficiency causes microcytosis, while vitamin B12, folate,




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Iron deficiency causes microcytosis, while vitamin B12, folate, and copper deficiency cause macrocytosis. If both iron deficiency and one of the other deficiencies are present, the MCV may be in the normal range, often with an increased red cell distribution width (RDW)
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how gelatinous necrosis. Anemia will improve with restored food intake. (See "Anorexia nervosa in adults and adolescents: Medical complications and their management", section on 'Hematologic'.) <span>Iron deficiency causes microcytosis, while vitamin B12, folate, and copper deficiency cause macrocytosis. If both iron deficiency and one of the other deficiencies are present, the MCV may be in the normal range, often with an increased red cell distribution width (RDW). Vitamin B12 and copper deficiency can cause other cytopenias; neutropenia commonly accompanies the anemia in copper deficiency. Vitamin B12 and copper deficiency both can produce poste




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Vitamin B12 and copper deficiency can cause other cytopenias; neutropenia commonly accompanies the anemia in copper deficiency. Vitamin B12 and copper deficiency both can produce posterior column neurologic abnormalities
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iciency cause macrocytosis. If both iron deficiency and one of the other deficiencies are present, the MCV may be in the normal range, often with an increased red cell distribution width (RDW). <span>Vitamin B12 and copper deficiency can cause other cytopenias; neutropenia commonly accompanies the anemia in copper deficiency. Vitamin B12 and copper deficiency both can produce posterior column neurologic abnormalities. The evaluation in all cases should include serum iron, transferrin/TIBC, ferritin, vitamin B12, and folate levels. Copper level should be measured in malnourished individuals with anem




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The evaluation in all cases should include serum iron, transferrin/TIBC, ferritin, vitamin B12, and folate levels. Copper level should be measured in malnourished individuals with anemia accompanied by neutropenia and/or neuropathy, as well as those with anemia in the setting of gastric/bariatric surgery or a history of zinc ingestion. Individuals with any of these deficiencies should be evaluated for the underlying cause
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iency can cause other cytopenias; neutropenia commonly accompanies the anemia in copper deficiency. Vitamin B12 and copper deficiency both can produce posterior column neurologic abnormalities. <span>The evaluation in all cases should include serum iron, transferrin/TIBC, ferritin, vitamin B12, and folate levels. Copper level should be measured in malnourished individuals with anemia accompanied by neutropenia and/or neuropathy, as well as those with anemia in the setting of gastric/bariatric surgery or a history of zinc ingestion. Individuals with any of these deficiencies should be evaluated for the underlying cause. Underlying systemic illness — Chronic anemia in patients with systemic illnesses may reflect anemia of chronic disease/inflammation (ACD/AI), particularly in disorders associated with




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Chronic anemia in patients with systemic illnesses may reflect anemia of chronic disease/inflammation (ACD/AI), particularly in disorders associated with inflammatory processes such as rheumatoid arthritis or systemic lupus erythematosus (SLE).

The reduction in hemoglobin is often mild to moderate. The red cells are typically normocytic, although there may occasionally be a moderate degree of microcytosis. Iron studies show decreased serum iron and normal or elevated ferritin concentrations. Serum erythropoietin is typically increased above the level seen in patients who are not anemic but to a lesser degree than would be observed in uncomplicated iron deficiency (figure 4). Serum hepcidin is not routinely available but would be expected to be elevated.

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n the setting of gastric/bariatric surgery or a history of zinc ingestion. Individuals with any of these deficiencies should be evaluated for the underlying cause. Underlying systemic illness — <span>Chronic anemia in patients with systemic illnesses may reflect anemia of chronic disease/inflammation (ACD/AI), particularly in disorders associated with inflammatory processes such as rheumatoid arthritis or systemic lupus erythematosus (SLE). The reduction in hemoglobin is often mild to moderate. The red cells are typically normocytic, although there may occasionally be a moderate degree of microcytosis. Iron studies show decreased serum iron and normal or elevated ferritin concentrations. Serum erythropoietin is typically increased above the level seen in patients who are not anemic but to a lesser degree than would be observed in uncomplicated iron deficiency (figure 4). Serum hepcidin is not routinely available but would be expected to be elevated. Underlying conditions commonly associated with ACD/AI include: ●Cancer ●Chronic kidney disease (may be associated with concomitant erythropoietin deficiency) ●Rheumatologic conditions ●




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Underlying conditions commonly associated with ACD/AI include:

● Cancer

● Chronic kidney disease (may be associated with concomitant erythropoietin deficiency)

● Rheumatologic conditions

● Hypothyroidism

● Infections

There is debate about whether diabetes mellitus per se causes ACD/AI, or whether ACD/AI can only be caused by complications of diabetes.

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nts who are not anemic but to a lesser degree than would be observed in uncomplicated iron deficiency (figure 4). Serum hepcidin is not routinely available but would be expected to be elevated. <span>Underlying conditions commonly associated with ACD/AI include: ●Cancer ●Chronic kidney disease (may be associated with concomitant erythropoietin deficiency) ●Rheumatologic conditions ●Hypothyroidism ●Infections There is debate about whether diabetes mellitus per se causes ACD/AI, or whether ACD/AI can only be caused by complications of diabetes. Studies attempting to distinguish between the two are lacking, and many individuals with diabetes have other comorbidities such as infection that could contribute to ACD/AI [34]. Anemia




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Pancytopenia is the combination of anemia, thrombocytopenia, and neutropenia (or leukopenia).
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those associated with pancytopenia, or if there are schistocytes (indicative of microangiopathic hemolysis) on the blood smear. (See 'Pancytopenia' below and 'Hemolysis' below.) Pancytopenia — <span>Pancytopenia is the combination of anemia, thrombocytopenia, and neutropenia (or leukopenia). Findings from peripheral blood smear examination are critical in the assessment of pancytopenia. Other testing is directed by the findings, as discussed separately. (See "Approach to th




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Findings of particular concern that warrant hematologist involvement and bone marrow examination include:

● Severe pancytopenia.

● Blasts or immature myeloid/lymphoid forms, which suggest acute leukemia.

● Abnormal lymphocytes (hairy cells, large granular lymphocytes, prolymphocytes).

● Leukoerythroblastosis (picture 10) with or without teardrop cells (dacrocytes; (picture 11)).

● Pancytopenia with hemolysis or thrombosis.

● Pancytopenia or bicytopenia (anemia with leukopenia or anemia with thrombocytopenia) in an older individual with normal vitamin B12, folate, and copper levels.

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eral blood smear examination are critical in the assessment of pancytopenia. Other testing is directed by the findings, as discussed separately. (See "Approach to the adult with pancytopenia".) <span>Findings of particular concern that warrant hematologist involvement and bone marrow examination include: ●Severe pancytopenia. ●Blasts or immature myeloid/lymphoid forms, which suggest acute leukemia. ●Abnormal lymphocytes (hairy cells, large granular lymphocytes, prolymphocytes). ●Leukoerythroblastosis (picture 10) with or without teardrop cells (dacrocytes; (picture 11)). ●Pancytopenia with hemolysis or thrombosis. ●Pancytopenia or bicytopenia (anemia with leukopenia or anemia with thrombocytopenia) in an older individual with normal vitamin B12, folate, and copper levels. Potential diagnoses are numerous (table 5). They include drug-induced pancytopenia (cytotoxic drugs, anti-infective drugs, anticonvulsants (table 6)), certain infections (viral [hepatit




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Potential diagnoses are numerous (table 5). They include drug-induced pancytopenia (cytotoxic drugs, anti-infective drugs, anticonvulsants (table 6)), certain infections (viral [hepatitis, cytomegalovirus, Epstein Barr virus] and severe non-viral [clostridial sepsis, malaria, leishmaniasis, leptospirosis, babesiosis]), bone marrow failure (aplastic anemia), myelodysplasia, myelofibrosis, clonal disorders such as paroxysmal nocturnal hemoglobinuria (PNH), and hematologic malignancies.
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ia with hemolysis or thrombosis. ●Pancytopenia or bicytopenia (anemia with leukopenia or anemia with thrombocytopenia) in an older individual with normal vitamin B12, folate, and copper levels. <span>Potential diagnoses are numerous (table 5). They include drug-induced pancytopenia (cytotoxic drugs, anti-infective drugs, anticonvulsants (table 6)), certain infections (viral [hepatitis, cytomegalovirus, Epstein Barr virus] and severe non-viral [clostridial sepsis, malaria, leishmaniasis, leptospirosis, babesiosis]), bone marrow failure (aplastic anemia), myelodysplasia, myelofibrosis, clonal disorders such as paroxysmal nocturnal hemoglobinuria (PNH), and hematologic malignancies. (See "Approach to the adult with pancytopenia" and "Aplastic anemia: Pathogenesis, clinical manifestations, and diagnosis", section on 'Differential diagnosis'.) These disorders can als




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Hypersplenism – Cirrhosis can cause pancytopenia due to sequestration of cells in the spleen (hypersplenism). Macrocytosis and target cells are often seen on the peripheral blood smear. The mean corpuscular volume (MCV) will typically be elevated to a moderate degree, usually no higher than 105 fL. Splenic imaging is appropriate if splenomegaly has not been previously documented.
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of paroxysmal nocturnal hemoglobinuria".) While a bone marrow disorder is always a consideration in individuals with pancytopenia, in some individuals, pancytopenia may be due to other causes: ●<span>Hypersplenism – Cirrhosis can cause pancytopenia due to sequestration of cells in the spleen (hypersplenism). Macrocytosis and target cells are often seen on the peripheral blood smear. The mean corpuscular volume (MCV) will typically be elevated to a moderate degree, usually no higher than 105 fL. Splenic imaging is appropriate if splenomegaly has not been previously documented. (See "Evaluation of splenomegaly and other splenic disorders in adults", section on 'Hypersplenism'.) ●Nutrient deficiency – Deficiency of vitamin B12, copper, and/or folate may also ca




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Nutrient deficiency – Deficiency of vitamin B12, copper, and/or folate may also cause pancytopenia and should be evaluated, especially if the peripheral blood smear shows macroovalocytes (picture 12), hypersegmented neutrophils (picture 13), and/or if the MCV is >110 fL.
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105 fL. Splenic imaging is appropriate if splenomegaly has not been previously documented. (See "Evaluation of splenomegaly and other splenic disorders in adults", section on 'Hypersplenism'.) ●<span>Nutrient deficiency – Deficiency of vitamin B12, copper, and/or folate may also cause pancytopenia and should be evaluated, especially if the peripheral blood smear shows macroovalocytes (picture 12), hypersegmented neutrophils (picture 13), and/or if the MCV is >110 fL. (See "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency".) ●Autoimmune – Autoimmune cytopenias typically affect a single cell line but can affect more than one




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Autoimmune – Autoimmune cytopenias typically affect a single cell line but can affect more than one cell line simultaneously, especially if there is an underlying rheumatologic disorder such as systemic lupus erythematosus (SLE) or a lymphoid disorder such as chronic lymphocytic leukemia (CLL)
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hows macroovalocytes (picture 12), hypersegmented neutrophils (picture 13), and/or if the MCV is >110 fL. (See "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency".) ●<span>Autoimmune – Autoimmune cytopenias typically affect a single cell line but can affect more than one cell line simultaneously, especially if there is an underlying rheumatologic disorder such as systemic lupus erythematosus (SLE) or a lymphoid disorder such as chronic lymphocytic leukemia (CLL). (See "Hematologic manifestations of systemic lupus erythematosus" and "Overview of the complications of chronic lymphocytic leukemia".) ●HLH – Hemophagocytic lymphohistiocytosis (HLH)




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HLH – Hemophagocytic lymphohistiocytosis (HLH) may be primary (typically in children) or secondary to an infection, malignancy, or rheumatologic condition.
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oid disorder such as chronic lymphocytic leukemia (CLL). (See "Hematologic manifestations of systemic lupus erythematosus" and "Overview of the complications of chronic lymphocytic leukemia".) ●<span>HLH – Hemophagocytic lymphohistiocytosis (HLH) may be primary (typically in children) or secondary to an infection, malignancy, or rheumatologic condition. (See "Clinical features and diagnosis of hemophagocytic lymphohistiocytosis".) ●TMAs – Thrombotic microangiopathies (TMAs) such as thrombotic thrombocytopenic purpura (TTP) typically ca




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TMAs – Thrombotic microangiopathies (TMAs) such as thrombotic thrombocytopenic purpura (TTP) typically cause thrombocytopenia and microangiopathic hemolytic anemia, with a very low platelet count and schistocytes on the blood smear. Some types of drug-induced TMAs such as due to quinine can cause pancytopenia. Disseminated intravascular coagulation (DIC) can cause pancytopenia due to TMA plus bone marrow suppression, with coagulation abnormalities often prominent.
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HLH) may be primary (typically in children) or secondary to an infection, malignancy, or rheumatologic condition. (See "Clinical features and diagnosis of hemophagocytic lymphohistiocytosis".) ●<span>TMAs – Thrombotic microangiopathies (TMAs) such as thrombotic thrombocytopenic purpura (TTP) typically cause thrombocytopenia and microangiopathic hemolytic anemia, with a very low platelet count and schistocytes on the blood smear. Some types of drug-induced TMAs such as due to quinine can cause pancytopenia. Disseminated intravascular coagulation (DIC) can cause pancytopenia due to TMA plus bone marrow suppression, with coagulation abnormalities often prominent. (See "Approach to the patient with suspected TTP, HUS, or other thrombotic microangiopathy (TMA)" and "Drug-induced thrombotic microangiopathy", section on 'Quinine' and "Disseminated i




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Reticulocyte count — Anemia can also be classified on the basis of reticulocyte production. This approach is most informative when the reticulocyte count is either very decreased or very elevated. Attention must be paid to the particular reticulocyte parameter reported (absolute count versus percentage) and is most helpful using a reticulocyte parameter that is corrected for the degree of anemia (table 2).
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r thrombotic microangiopathy (TMA)" and "Drug-induced thrombotic microangiopathy", section on 'Quinine' and "Disseminated intravascular coagulation (DIC) in adults: Evaluation and management".) <span>Reticulocyte count — Anemia can also be classified on the basis of reticulocyte production. This approach is most informative when the reticulocyte count is either very decreased or very elevated. Attention must be paid to the particular reticulocyte parameter reported (absolute count versus percentage) and is most helpful using a reticulocyte parameter that is corrected for the degree of anemia (table 2). (See 'Reticulocyte production' above.) Reticulocytosis requires a normally functioning bone marrow replete with iron, folate, cobalamin (vitamin B12), and copper, and a normally functio




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Reticulocytosis requires a normally functioning bone marrow replete with iron, folate, cobalamin (vitamin B12), and copper, and a normally functioning kidney that can sense a decrease in oxygen delivery and produce a compensatory increase in erythropoietin (EPO). Thus, a decreased reticulocyte count suggests underproduction of red blood cells (RBCs; bone marrow suppression), and an increased reticulocyte count usually suggests hemolysis or blood loss. If both bone marrow suppression and hemolysis or blood loss are present, the reticulocyte count will be inappropriately low
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meter reported (absolute count versus percentage) and is most helpful using a reticulocyte parameter that is corrected for the degree of anemia (table 2). (See 'Reticulocyte production' above.) <span>Reticulocytosis requires a normally functioning bone marrow replete with iron, folate, cobalamin (vitamin B12), and copper, and a normally functioning kidney that can sense a decrease in oxygen delivery and produce a compensatory increase in erythropoietin (EPO). Thus, a decreased reticulocyte count suggests underproduction of red blood cells (RBCs; bone marrow suppression), and an increased reticulocyte count usually suggests hemolysis or blood loss. If both bone marrow suppression and hemolysis or blood loss are present, the reticulocyte count will be inappropriately low. ●Causes •Decreased – Anemia with a decreased (or inappropriately low) reticulocyte count may be due to: -Deficiency of iron, vitamin B12, folate, or copper -Medications that suppress t




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Anemia with a decreased (or inappropriately low) reticulocyte count may be due to:

- Deficiency of iron, vitamin B12, folate, or copper

- Medications that suppress the bone marrow

- Primary bone marrow disorders including myelodysplastic syndrome (MDS), myelofibrosis, or leukemia

- Very recent bleeding (within five to seven days, before bone marrow compensation has occurred)

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count usually suggests hemolysis or blood loss. If both bone marrow suppression and hemolysis or blood loss are present, the reticulocyte count will be inappropriately low. ●Causes •Decreased – <span>Anemia with a decreased (or inappropriately low) reticulocyte count may be due to: -Deficiency of iron, vitamin B12, folate, or copper -Medications that suppress the bone marrow -Primary bone marrow disorders including myelodysplastic syndrome (MDS), myelofibrosis, or leukemia -Very recent bleeding (within five to seven days, before bone marrow compensation has occurred) •Increased – Anemia with an increased reticulocyte count may be due to: -Hemolysis -Repletion of deficient iron, vitamin B12, folate, or copper (early phase of recovery) -Recovery from




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Anemia with an increased reticulocyte count may be due to:

- Hemolysis

- Repletion of deficient iron, vitamin B12, folate, or copper (early phase of recovery)

- Recovery from bleeding

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arrow disorders including myelodysplastic syndrome (MDS), myelofibrosis, or leukemia -Very recent bleeding (within five to seven days, before bone marrow compensation has occurred) •Increased – <span>Anemia with an increased reticulocyte count may be due to: -Hemolysis -Repletion of deficient iron, vitamin B12, folate, or copper (early phase of recovery) -Recovery from bleeding Regardless of other causes of anemia, an insufficient increase in the reticulocyte count suggests that the function of the bone marrow and/or the kidney are impaired. ●Evaluation – If t




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If the reticulocyte count is increased and the cause of anemia is not readily apparent, additional laboratory testing for hemolysis is appropriate (table 3).
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rom bleeding Regardless of other causes of anemia, an insufficient increase in the reticulocyte count suggests that the function of the bone marrow and/or the kidney are impaired. ●Evaluation – <span>If the reticulocyte count is increased and the cause of anemia is not readily apparent, additional laboratory testing for hemolysis is appropriate (table 3). (See 'Hemolysis' below.) ●Response to treatment – An increase in reticulocyte count following treatment can also be very helpful in determining if the cause of anemia was determined acc




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An increase in reticulocyte count following treatment can also be very helpful in determining if the cause of anemia was determined accurately and completely. As examples:

• If anemia was attributed to a deficiency (iron, vitamin B12, folate), brisk reticulocytosis is expected to occur within one to two weeks of repletion.

• If the reticulocyte count does not increase with correction of a deficiency, this suggests an additional cause of anemia is interfering with bone marrow function. As an example, vitamin B12 or folate deficiency may occur concurrently with iron deficiency, causing a normocytic anemia (see 'Normocytic (normal MCV)' below). This combination of findings is often seen in malabsorption syndromes such as for celiac disease, autoimmune gastritis, or bariatric surgery.

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ocyte count is increased and the cause of anemia is not readily apparent, additional laboratory testing for hemolysis is appropriate (table 3). (See 'Hemolysis' below.) ●Response to treatment – <span>An increase in reticulocyte count following treatment can also be very helpful in determining if the cause of anemia was determined accurately and completely. As examples: •If anemia was attributed to a deficiency (iron, vitamin B12, folate), brisk reticulocytosis is expected to occur within one to two weeks of repletion. •If the reticulocyte count does not increase with correction of a deficiency, this suggests an additional cause of anemia is interfering with bone marrow function. As an example, vitamin B12 or folate deficiency may occur concurrently with iron deficiency, causing a normocytic anemia (see 'Normocytic (normal MCV)' below). This combination of findings is often seen in malabsorption syndromes such as for celiac disease, autoimmune gastritis, or bariatric surgery. (See 'Malabsorption/malnutrition' above.) Hemolysis — Hemolytic anemia should be considered when there is a rapid fall in hemoglobin concentration with an increased reticulocyte count i




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Hemolytic anemia should be considered when there is a rapid fall in hemoglobin concentration with an increased reticulocyte count in the absence of blood loss (table 2). Other abnormal laboratory findings indicative of hemolysis are summarized in the table (table 3).

Schistocytes on the blood smear indicated likely hemolysis due to mechanical RBC destruction. Schistocytes plus thrombocytopenia indicate possible thrombotic microangiopathy (TMA), which may be life-threatening.

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is combination of findings is often seen in malabsorption syndromes such as for celiac disease, autoimmune gastritis, or bariatric surgery. (See 'Malabsorption/malnutrition' above.) Hemolysis — <span>Hemolytic anemia should be considered when there is a rapid fall in hemoglobin concentration with an increased reticulocyte count in the absence of blood loss (table 2). Other abnormal laboratory findings indicative of hemolysis are summarized in the table (table 3). Schistocytes on the blood smear indicated likely hemolysis due to mechanical RBC destruction. Schistocytes plus thrombocytopenia indicate possible thrombotic microangiopathy (TMA), which may be life-threatening. (See "Approach to the patient with suspected TTP, HUS, or other thrombotic microangiopathy (TMA)".) Chronic hemolysis may present with a stable hemoglobin, a high reticulocyte count, an




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Chronic hemolysis may present with a stable hemoglobin, a high reticulocyte count, and a normal lactate dehydrogenase (LDH) and bilirubin. The combination of an increased LDH and reduced haptoglobin is 90 percent specific for acute hemolysis, while the combination of a normal LDH and a serum haptoglobin greater than 25 mg/dL is 92 percent sensitive for ruling out hemolysis [36,37].

Intramedullary hemolysis (within the bone marrow) due to ineffective erythropoiesis, as may be seen in thalassemia or vitamin B12 deficiency, may produce elevations of bilirubin and LDH without reticulocytosis

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ocytopenia indicate possible thrombotic microangiopathy (TMA), which may be life-threatening. (See "Approach to the patient with suspected TTP, HUS, or other thrombotic microangiopathy (TMA)".) <span>Chronic hemolysis may present with a stable hemoglobin, a high reticulocyte count, and a normal lactate dehydrogenase (LDH) and bilirubin. The combination of an increased LDH and reduced haptoglobin is 90 percent specific for acute hemolysis, while the combination of a normal LDH and a serum haptoglobin greater than 25 mg/dL is 92 percent sensitive for ruling out hemolysis [36,37]. Intramedullary hemolysis (within the bone marrow) due to ineffective erythropoiesis, as may be seen in thalassemia or vitamin B12 deficiency, may produce elevations of bilirubin and LDH without reticulocytosis. Causes of hemolysis are numerous and can be categorized in several ways, as summarized in the table (table 7) and discussed in more detail separately. (See "Diagnosis of hemolytic anem




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Causes of hemolysis are numerous and can be categorized in several ways, as summarized in the table (table 7) and discussed in more detail separately. (See "Diagnosis of hemolytic anemia in adults".)
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molysis (within the bone marrow) due to ineffective erythropoiesis, as may be seen in thalassemia or vitamin B12 deficiency, may produce elevations of bilirubin and LDH without reticulocytosis. <span>Causes of hemolysis are numerous and can be categorized in several ways, as summarized in the table (table 7) and discussed in more detail separately. (See "Diagnosis of hemolytic anemia in adults".) These include: ●Hereditary, non-immune: •Hemoglobinopathies (sickle cell disease, thalassemias, unstable hemoglobins) •Hereditary red cell enzyme deficiencies (glucose-6-phosphate dehyd




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Hereditary, non-immune:

• Hemoglobinopathies (sickle cell disease, thalassemias, unstable hemoglobins)

• Hereditary red cell enzyme deficiencies (glucose-6-phosphate dehydrogenase [G6PD], pyruvate kinase [PK], glucose phosphate isomerase, 5’ nucleotidase)

• Hereditary RBC membrane defects (hereditary spherocytosis [HS], elliptocytosis [HE], stomatocytosis [HSt])

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e numerous and can be categorized in several ways, as summarized in the table (table 7) and discussed in more detail separately. (See "Diagnosis of hemolytic anemia in adults".) These include: ●<span>Hereditary, non-immune: •Hemoglobinopathies (sickle cell disease, thalassemias, unstable hemoglobins) •Hereditary red cell enzyme deficiencies (glucose-6-phosphate dehydrogenase [G6PD], pyruvate kinase [PK], glucose phosphate isomerase, 5’ nucleotidase) •Hereditary RBC membrane defects (hereditary spherocytosis [HS], elliptocytosis [HE], stomatocytosis [HSt]) ●Acquired, non-immune •Membrane defects (liver disease, acquired acanthocytosis) •Infections (malaria, babesiosis, clostridial sepsis, Bartonellosis, trypanosomiasis, visceral leishmani




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Acquired, non-immune

• Membrane defects (liver disease, acquired acanthocytosis)

• Infections (malaria, babesiosis, clostridial sepsis, Bartonellosis, trypanosomiasis, visceral leishmaniasis)

• Drug-induced (oxidant stress)

• Severe burns

• Thrombotic microangiopathies (thrombotic thrombocytopenic purpura [TTP], hemolytic uremic syndrome [HUS], drug-induced TMA)

• Mechanical (intravascular devices, artificial heart valve, giant hemangioma, footstrike hemolysis)

• Hypersplenism (may have a component of phagocytosis but is not antibody mediated)

• Vasculitis

• Severe hypertension

• Heavy metals (Wilson disease, copper toxicity, arsine toxicity)

• Envenomation (snake, brown recluse spider, hobo spider)

• Hypophosphatemia

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rogenase [G6PD], pyruvate kinase [PK], glucose phosphate isomerase, 5’ nucleotidase) •Hereditary RBC membrane defects (hereditary spherocytosis [HS], elliptocytosis [HE], stomatocytosis [HSt]) ●<span>Acquired, non-immune •Membrane defects (liver disease, acquired acanthocytosis) •Infections (malaria, babesiosis, clostridial sepsis, Bartonellosis, trypanosomiasis, visceral leishmaniasis) •Drug-induced (oxidant stress) •Severe burns •Thrombotic microangiopathies (thrombotic thrombocytopenic purpura [TTP], hemolytic uremic syndrome [HUS], drug-induced TMA) •Mechanical (intravascular devices, artificial heart valve, giant hemangioma, footstrike hemolysis) •Hypersplenism (may have a component of phagocytosis but is not antibody mediated) •Vasculitis •Severe hypertension •Heavy metals (Wilson disease, copper toxicity, arsine toxicity) •Envenomation (snake, brown recluse spider, hobo spider) •Hypophosphatemia ●Acquired, immune-mediated •Autoimmune (warm autoimmune hemolytic anemia [AIHA], cold agglutinin disease, paroxysmal cold hemoglobinuria) •Hemolytic transfusion reactions •Drug-induced




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Acquired, immune-mediated

• Autoimmune (warm autoimmune hemolytic anemia [AIHA], cold agglutinin disease, paroxysmal cold hemoglobinuria)

• Hemolytic transfusion reactions

• Drug-induced

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antibody mediated) •Vasculitis •Severe hypertension •Heavy metals (Wilson disease, copper toxicity, arsine toxicity) •Envenomation (snake, brown recluse spider, hobo spider) •Hypophosphatemia ●<span>Acquired, immune-mediated •Autoimmune (warm autoimmune hemolytic anemia [AIHA], cold agglutinin disease, paroxysmal cold hemoglobinuria) •Hemolytic transfusion reactions •Drug-induced Once hemolysis is confirmed, the specific cause must be identified to ensure appropriate management. Details of the evaluation are discussed in a separate topic review. (See "Diagnosis




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Many individuals with anemia will be otherwise well, and the clinical history and other initial findings on the complete blood count (CBC) may not be helpful for suggesting specific diagnoses leading to anemia. A diagnostic approach based on the mean corpuscular volume (MCV) is most useful in these cases, as illustrated in the flowchart (algorithm 1).
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iate management. Details of the evaluation are discussed in a separate topic review. (See "Diagnosis of hemolytic anemia in adults", section on 'Diagnostic approach'.) EVALUATION BASED ON MCV — <span>Many individuals with anemia will be otherwise well, and the clinical history and other initial findings on the complete blood count (CBC) may not be helpful for suggesting specific diagnoses leading to anemia. A diagnostic approach based on the mean corpuscular volume (MCV) is most useful in these cases, as illustrated in the flowchart (algorithm 1). Evaluation of anemia using the MCV is especially useful for microcytic and macrocytic anemia. (See 'Microcytosis (low MCV)' below and 'Normocytic (normal MCV)' below.) Microcytosis (low




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A decreased MCV (usually <80 fL) reflects a defect in cellular hemoglobin synthesis. These anemias are summarized in the table (table 8) and discussed in detail separately and briefly below.
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Evaluation of anemia using the MCV is especially useful for microcytic and macrocytic anemia. (See 'Microcytosis (low MCV)' below and 'Normocytic (normal MCV)' below.) Microcytosis (low MCV) — <span>A decreased MCV (usually <80 fL) reflects a defect in cellular hemoglobin synthesis. These anemias are summarized in the table (table 8) and discussed in detail separately and briefly below. (See "Microcytosis/Microcytic anemia".) ●Causes •Iron deficiency – Restricted iron availability (iron deficiency and some cases of anemia of chronic disease/anemia of inflammation [ACD/




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Causes

Iron deficiency – Restricted iron availability (iron deficiency and some cases of anemia of chronic disease/anemia of inflammation [ACD/AI], which can cause functional iron deficiency). (See "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults" and "Anemia of chronic disease/anemia of inflammation".)

Decreased globin chains – Qualitative abnormalities in globin proteins such as thalassemia, hemoglobin (Hb) C, and HbE (but not HbS). (See "Pathophysiology of thalassemia" and "Clinical manifestations and diagnosis of the thalassemias" and "Overview of variant sickle cell syndromes".)

Decreased heme – Abnormalities of the heme porphyrin ring, including sideroblastic anemias and lead poisoning. (See "Causes and pathophysiology of the sideroblastic anemias" and "Lead exposure and poisoning in adults".)

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cts a defect in cellular hemoglobin synthesis. These anemias are summarized in the table (table 8) and discussed in detail separately and briefly below. (See "Microcytosis/Microcytic anemia".) ●<span>Causes •Iron deficiency – Restricted iron availability (iron deficiency and some cases of anemia of chronic disease/anemia of inflammation [ACD/AI], which can cause functional iron deficiency). (See "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults" and "Anemia of chronic disease/anemia of inflammation".) •Decreased globin chains – Qualitative abnormalities in globin proteins such as thalassemia, hemoglobin (Hb) C, and HbE (but not HbS). (See "Pathophysiology of thalassemia" and "Clinical manifestations and diagnosis of the thalassemias" and "Overview of variant sickle cell syndromes".) •Decreased heme – Abnormalities of the heme porphyrin ring, including sideroblastic anemias and lead poisoning. (See "Causes and pathophysiology of the sideroblastic anemias" and "Lead exposure and poisoning in adults".) ●Very low MCV – Iron deficiency and thalassemia are the most likely causes of a very low MCV (<80 fL). The ratio of the MCV to the red blood cell (RBC) count (Mentzer index) is usefu




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Very low MCV – Iron deficiency and thalassemia are the most likely causes of a very low MCV (<80 fL). The ratio of the MCV to the red blood cell (RBC) count (Mentzer index) is useful in predicting the likelihood of thalassemia trait versus iron deficiency. If the ratio of MCV (in fL) to RBC count (in millions of cells/microL) is less than 13, thalassemia is more likely than iron deficiency [38].

In practice, all individuals with a low MCV should have iron studies to evaluate iron status (and should have deficiency corrected if present), because the results of hemoglobin analysis can be altered by concomitant iron deficiency.

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ies of the heme porphyrin ring, including sideroblastic anemias and lead poisoning. (See "Causes and pathophysiology of the sideroblastic anemias" and "Lead exposure and poisoning in adults".) ●<span>Very low MCV – Iron deficiency and thalassemia are the most likely causes of a very low MCV (<80 fL). The ratio of the MCV to the red blood cell (RBC) count (Mentzer index) is useful in predicting the likelihood of thalassemia trait versus iron deficiency. If the ratio of MCV (in fL) to RBC count (in millions of cells/microL) is less than 13, thalassemia is more likely than iron deficiency [38]. In practice, all individuals with a low MCV should have iron studies to evaluate iron status (and should have deficiency corrected if present), because the results of hemoglobin analysis can be altered by concomitant iron deficiency. (See "Methods for hemoglobin analysis and hemoglobinopathy testing", section on 'Patient with suspected thalassemia'.) ●Evaluation •All patients – All patients with microcytic anemia sh




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All patients – All patients with microcytic anemia should have serum iron, total iron binding capacity (TIBC)/transferrin, and serum ferritin concentrations measured, with calculated transferrin saturation (TSAT). Iron studies will identify iron deficiency (the most likely diagnosis for microcytic anemia) and ACD/AI in most cases. Mild microcytosis with iron studies showing low iron, low TIBC, and high-normal to high ferritin in the appropriate clinical context (eg, chronic inflammatory condition with normal MCV prior to its development) is consistent with ACD/AI.
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lobin analysis can be altered by concomitant iron deficiency. (See "Methods for hemoglobin analysis and hemoglobinopathy testing", section on 'Patient with suspected thalassemia'.) ●Evaluation •<span>All patients – All patients with microcytic anemia should have serum iron, total iron binding capacity (TIBC)/transferrin, and serum ferritin concentrations measured, with calculated transferrin saturation (TSAT). Iron studies will identify iron deficiency (the most likely diagnosis for microcytic anemia) and ACD/AI in most cases. Mild microcytosis with iron studies showing low iron, low TIBC, and high-normal to high ferritin in the appropriate clinical context (eg, chronic inflammatory condition with normal MCV prior to its development) is consistent with ACD/AI. (See "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults", section on 'Iron studies (list of available tests)'.) •Individuals with normal iron studies – Hemogl




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Individuals with normal iron studies – Hemoglobin quantitation should be ordered in individuals with microcytic anemia who do not have iron deficiency or ACD/AI to identify beta thalassemia or other hemoglobinopathies. Globin gene studies may be needed to diagnose alpha thalassemia; the family history may be helpful in determining likelihood of these disorders. Minimal to mild anemia and microcytosis may indicate non-transfusion-dependent thalassemia (thalassemia trait). Basophilic stippling may also be seen with beta thalassemia [39].
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prior to its development) is consistent with ACD/AI. (See "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults", section on 'Iron studies (list of available tests)'.) •<span>Individuals with normal iron studies – Hemoglobin quantitation should be ordered in individuals with microcytic anemia who do not have iron deficiency or ACD/AI to identify beta thalassemia or other hemoglobinopathies. Globin gene studies may be needed to diagnose alpha thalassemia; the family history may be helpful in determining likelihood of these disorders. Minimal to mild anemia and microcytosis may indicate non-transfusion-dependent thalassemia (thalassemia trait). Basophilic stippling may also be seen with beta thalassemia [39]. (See "Methods for hemoglobin analysis and hemoglobinopathy testing".) •Individuals with normal hemoglobin – Basophilic stippling (picture 14) suggests possible lead poisoning, and whole




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Individuals with normal hemoglobin – Basophilic stippling (picture 14) suggests possible lead poisoning, and whole blood lead levels should be measured. The diagnosis of sideroblastic anemia requires a bone marrow examination.
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n-transfusion-dependent thalassemia (thalassemia trait). Basophilic stippling may also be seen with beta thalassemia [39]. (See "Methods for hemoglobin analysis and hemoglobinopathy testing".) •<span>Individuals with normal hemoglobin – Basophilic stippling (picture 14) suggests possible lead poisoning, and whole blood lead levels should be measured. The diagnosis of sideroblastic anemia requires a bone marrow examination. (See "Bone marrow aspiration and biopsy: Indications and technique", section on 'Indications' and "Evaluation of bone marrow aspirate smears".) Macrocytosis (high MCV) — An increased MC




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Macrocytosis (high MCV) — An increased MCV (>100 fL) is typically attributed to asynchronous maturation of nuclear chromatin, although other causes may also be present. These anemias are summarized in the table (table 9) and discussed in detail separately and briefly below.
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lastic anemia requires a bone marrow examination. (See "Bone marrow aspiration and biopsy: Indications and technique", section on 'Indications' and "Evaluation of bone marrow aspirate smears".) <span>Macrocytosis (high MCV) — An increased MCV (>100 fL) is typically attributed to asynchronous maturation of nuclear chromatin, although other causes may also be present. These anemias are summarized in the table (table 9) and discussed in detail separately and briefly below. (See "Macrocytosis/Macrocytic anemia".) ●Causes •Megaloblastic anemia – Asynchronous nuclear maturation (megaloblastosis), in which the rate of cell division is reduced relative to cyto




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Megaloblastic anemia – Asynchronous nuclear maturation (megaloblastosis), in which the rate of cell division is reduced relative to cytoplasmic expansion. (See "Macrocytosis/Macrocytic anemia", section on 'Megaloblastic anemia'.)

Megaloblastic maturation can be due to:

- Vitamin B12 deficiency

- Folate deficiency

- Copper deficiency

- Myelodysplastic syndrome (MDS)

- Aplastic anemia

- Diamond Blackfan anemia

- Drugs that interfere with DNA synthesis

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ough other causes may also be present. These anemias are summarized in the table (table 9) and discussed in detail separately and briefly below. (See "Macrocytosis/Macrocytic anemia".) ●Causes •<span>Megaloblastic anemia – Asynchronous nuclear maturation (megaloblastosis), in which the rate of cell division is reduced relative to cytoplasmic expansion. (See "Macrocytosis/Macrocytic anemia", section on 'Megaloblastic anemia'.) Megaloblastic maturation can be due to: -Vitamin B12 deficiency -Folate deficiency -Copper deficiency -Myelodysplastic syndrome (MDS) -Aplastic anemia -Diamond Blackfan anemia -Drugs that interfere with DNA synthesis •Membrane changes – In some cases, conditions that increase RBC membrane (such as liver disease or excess alcohol [even without liver disease]) and other underlying disorders such as hy




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Membrane changes – In some cases, conditions that increase RBC membrane (such as liver disease or excess alcohol [even without liver disease]) and other underlying disorders such as hypothyroidism can cause increases in MCV. Stomatocytosis (hereditary or acquired) can also cause macrocytic anemia.
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can be due to: -Vitamin B12 deficiency -Folate deficiency -Copper deficiency -Myelodysplastic syndrome (MDS) -Aplastic anemia -Diamond Blackfan anemia -Drugs that interfere with DNA synthesis •<span>Membrane changes – In some cases, conditions that increase RBC membrane (such as liver disease or excess alcohol [even without liver disease]) and other underlying disorders such as hypothyroidism can cause increases in MCV. Stomatocytosis (hereditary or acquired) can also cause macrocytic anemia. (See "Macrocytosis/Macrocytic anemia", section on 'Causes of macrocytosis/macrocytic anemia'.) •Reticulocytosis – Reticulocytes are larger than mature RBCs (picture 3), and reticulocyto




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Reticulocytosis – Reticulocytes are larger than mature RBCs (picture 3), and reticulocytosis will increase the MCV. This will be associated with an increased red cell distribution width (RDW) and can often be suspected from examination of the peripheral blood smear.
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cause increases in MCV. Stomatocytosis (hereditary or acquired) can also cause macrocytic anemia. (See "Macrocytosis/Macrocytic anemia", section on 'Causes of macrocytosis/macrocytic anemia'.) •<span>Reticulocytosis – Reticulocytes are larger than mature RBCs (picture 3), and reticulocytosis will increase the MCV. This will be associated with an increased red cell distribution width (RDW) and can often be suspected from examination of the peripheral blood smear. (See 'Reticulocyte production' above.) Reticulocytes may be increased in: -Hemolytic anemias (acute or chronic) -Recovery from bleeding -Repletion of iron or other deficient nutrient -R




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Spurious – Increased concentrations of immunoglobulin or acute phase proteins such as occurs with inflammation or a polyclonal or monoclonal gammopathy may cause small rouleaux (picture 15) that are counted by electronic counters as single large cells. This is a laboratory artifact that can be assessed by viewing the peripheral blood smear.
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increased in: -Hemolytic anemias (acute or chronic) -Recovery from bleeding -Repletion of iron or other deficient nutrient -Recovery from bone marrow suppression such as binge drinking alcohol •<span>Spurious – Increased concentrations of immunoglobulin or acute phase proteins such as occurs with inflammation or a polyclonal or monoclonal gammopathy may cause small rouleaux (picture 15) that are counted by electronic counters as single large cells. This is a laboratory artifact that can be assessed by viewing the peripheral blood smear. ●Evaluation •All individuals – Serum vitamin B12 level should be measured in all patients with unevaluated macrocytosis. All individuals who are nutritionally compromised or who have ha




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All individuals – Serum vitamin B12 level should be measured in all patients with unevaluated macrocytosis. All individuals who are nutritionally compromised or who have had gastric surgery should also have serum folate measured. In patients without known nutritional/gastric issues who have MCV >110 fL and a normal vitamin B12 level, serum methylmalonic acid (MMA) and serum folate should be measured.
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small rouleaux (picture 15) that are counted by electronic counters as single large cells. This is a laboratory artifact that can be assessed by viewing the peripheral blood smear. ●Evaluation •<span>All individuals – Serum vitamin B12 level should be measured in all patients with unevaluated macrocytosis. All individuals who are nutritionally compromised or who have had gastric surgery should also have serum folate measured. In patients without known nutritional/gastric issues who have MCV >110 fL and a normal vitamin B12 level, serum methylmalonic acid (MMA) and serum folate should be measured. (See "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency", section on 'Diagnostic evaluation'.) •Individuals with normal vitamin B12 and folate -Thyroid stimulat




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Individuals with normal vitamin B12 and folate

- Thyroid stimulating hormone (TSH) should be checked. (See "Macrocytosis/Macrocytic anemia", section on 'Hypothyroidism'.)

- Alcohol use should be assessed. The MCV typically is not >105 fL in alcohol-induced macrocytosis. (See "Hematologic complications of alcohol use", section on 'Anemia'.)

- Serum copper level should be checked, especially if neutropenia and/or neuropathy are present or if the history reveals zinc ingestion or other risk factors. (See "Copper deficiency myeloneuropathy", section on 'Causes of acquired copper deficiency'.)

- The peripheral blood smear (or report) should be reviewed. If the blood smear shows target cells, liver synthetic tests should be measured. The MCV in liver disease typically is not >105 fL. Other morphologic abnormalities such as stomatocytosis should be evaluated, if present. If the copper level is normal and the blood smear shows evidence of dysplasia such as bilobed or immature neutrophils or binucleate RBCs, or other cytopenias, refer to a hematologist for bone marrow and/or molecular (DNA) studies on bone marrow or peripheral blood.

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vel, serum methylmalonic acid (MMA) and serum folate should be measured. (See "Clinical manifestations and diagnosis of vitamin B12 and folate deficiency", section on 'Diagnostic evaluation'.) •<span>Individuals with normal vitamin B12 and folate -Thyroid stimulating hormone (TSH) should be checked. (See "Macrocytosis/Macrocytic anemia", section on 'Hypothyroidism'.) -Alcohol use should be assessed. The MCV typically is not >105 fL in alcohol-induced macrocytosis. (See "Hematologic complications of alcohol use", section on 'Anemia'.) -Serum copper level should be checked, especially if neutropenia and/or neuropathy are present or if the history reveals zinc ingestion or other risk factors. (See "Copper deficiency myeloneuropathy", section on 'Causes of acquired copper deficiency'.) -The peripheral blood smear (or report) should be reviewed. If the blood smear shows target cells, liver synthetic tests should be measured. The MCV in liver disease typically is not >105 fL. Other morphologic abnormalities such as stomatocytosis should be evaluated, if present. If the copper level is normal and the blood smear shows evidence of dysplasia such as bilobed or immature neutrophils or binucleate RBCs, or other cytopenias, refer to a hematologist for bone marrow and/or molecular (DNA) studies on bone marrow or peripheral blood. (See "Clinical manifestations and diagnosis of myelodysplastic syndromes (MDS)".) Normocytic (normal MCV) — A normal MCV (80 to 100 fL) is the most common finding in anemic men and post




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A normal MCV (80 to 100 fL) is the most common finding in anemic men and postmenopausal women. Normocytic anemias can be more challenging to evaluate than anemias with an MCV that is obviously low or high. Causes are more numerous and may be multifactorial, an underlying condition may not be apparent, and other findings may be nonspecific
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st for bone marrow and/or molecular (DNA) studies on bone marrow or peripheral blood. (See "Clinical manifestations and diagnosis of myelodysplastic syndromes (MDS)".) Normocytic (normal MCV) — <span>A normal MCV (80 to 100 fL) is the most common finding in anemic men and postmenopausal women. Normocytic anemias can be more challenging to evaluate than anemias with an MCV that is obviously low or high. Causes are more numerous and may be multifactorial, an underlying condition may not be apparent, and other findings may be nonspecific. Often normocytic anemia is associated with a slightly elevated RDW, and the reticulocyte count is not substantially increased (and may be decreased). An increased RDW may indicate a po




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Often normocytic anemia is associated with a slightly elevated RDW, and the reticulocyte count is not substantially increased (and may be decreased). An increased RDW may indicate a population of microcytic or macrocytic RBCs that is too small to shift the MCV out of the normal range, or combined microcytic and macrocytic processes, such as iron deficiency plus vitamin B12 or folate deficiency [40]
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e than anemias with an MCV that is obviously low or high. Causes are more numerous and may be multifactorial, an underlying condition may not be apparent, and other findings may be nonspecific. <span>Often normocytic anemia is associated with a slightly elevated RDW, and the reticulocyte count is not substantially increased (and may be decreased). An increased RDW may indicate a population of microcytic or macrocytic RBCs that is too small to shift the MCV out of the normal range, or combined microcytic and macrocytic processes, such as iron deficiency plus vitamin B12 or folate deficiency [40]. ●Causes •Nutrient deficiency – Any of the causes of acquired microcytic or macrocytic anemia, especially early stages of deficiency of iron, vitamin B12, folate, or copper. (See 'Micro




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Nutrient deficiency – Any of the causes of acquired microcytic or macrocytic anemia, especially early stages of deficiency of iron, vitamin B12, folate, or copper.
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ic RBCs that is too small to shift the MCV out of the normal range, or combined microcytic and macrocytic processes, such as iron deficiency plus vitamin B12 or folate deficiency [40]. ●Causes •<span>Nutrient deficiency – Any of the causes of acquired microcytic or macrocytic anemia, especially early stages of deficiency of iron, vitamin B12, folate, or copper. (See 'Microcytosis (low MCV)' above and 'Macrocytosis (high MCV)' above.) •Multiple causes – Combined microcytic plus macrocytic anemia [40]. The most characteristic situation is simult




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Multiple causes – Combined microcytic plus macrocytic anemia [40]. The most characteristic situation is simultaneous deficiency of vitamin B12 and iron in an individual with celiac disease or autoimmune gastritis.
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quired microcytic or macrocytic anemia, especially early stages of deficiency of iron, vitamin B12, folate, or copper. (See 'Microcytosis (low MCV)' above and 'Macrocytosis (high MCV)' above.) •<span>Multiple causes – Combined microcytic plus macrocytic anemia [40]. The most characteristic situation is simultaneous deficiency of vitamin B12 and iron in an individual with celiac disease or autoimmune gastritis. (See "Epidemiology, pathogenesis, and clinical manifestations of celiac disease in adults" and "Metaplastic (chronic) atrophic gastritis".) Hemolytic anemia without marked reticulocytos




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ACD/AI – Anemia of chronic disease/anemia of inflammation (ACD/AI). (See "Anemia of chronic disease/anemia of inflammation".)

CDK – Anemia of chronic kidney disease (CKD). (See "Overview of the management of chronic kidney disease in adults", section on 'Anemia'.)

HF – Anemia of heart failure (HF), including cardio-renal syndrome [41]. (See "Evaluation and management of anemia and iron deficiency in adults with heart failure" and "Cardiorenal syndrome: Definition, prevalence, diagnosis, and pathophysiology".)

Endocrine – Anemia with endocrine deficiency, including hypothyroidism (most cases), androgen deficiency, or adrenal insufficiency (in adrenal insufficiency, anemia may be masked by volume contraction). (See 'Caveats for normal ranges' above and "Clinical manifestations of adrenal insufficiency in adults", section on 'Hematologic findings'.)

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without marked reticulocytosis (due to concomitant bone marrow suppression from another cause). (See "Diagnosis of hemolytic anemia in adults", section on 'Hemolysis without reticulocytosis'.) <span>•ACD/AI – Anemia of chronic disease/anemia of inflammation (ACD/AI). (See "Anemia of chronic disease/anemia of inflammation".) •CDK – Anemia of chronic kidney disease (CKD). (See "Overview of the management of chronic kidney disease in adults", section on 'Anemia'.) •HF – Anemia of heart failure (HF), including cardio-renal syndrome [41]. (See "Evaluation and management of anemia and iron deficiency in adults with heart failure" and "Cardiorenal syndrome: Definition, prevalence, diagnosis, and pathophysiology".) •Endocrine – Anemia with endocrine deficiency, including hypothyroidism (most cases), androgen deficiency, or adrenal insufficiency (in adrenal insufficiency, anemia may be masked by volume contraction). (See 'Caveats for normal ranges' above and "Clinical manifestations of adrenal insufficiency in adults", section on 'Hematologic findings'.) •Cancer – Cancer-associated anemia, including monoclonal gammopathies. (See "Causes of anemia in patients with cancer".) •Clonal hematopoietic stem cell disorders – Anemia due to a clonal




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Clonal hematopoietic stem cell disorders – Anemia due to a clonal disorder of erythropoiesis (myelodysplastic syndrome, aplastic anemia, or clonal cytopenias of uncertain significance [CCUS]) [42]. The strict definition of clonal hematopoiesis of indeterminate potential (CHIP) includes normal hemoglobin and other blood counts. (See "Clinical manifestations and diagnosis of myelodysplastic syndromes (MDS)" and "Idiopathic and clonal cytopenias of uncertain significance (ICUS and CCUS)".)

Early blood loss – Blood loss that has not yet caused iron deficiency. (See "Evaluation of occult gastrointestinal bleeding".)

PRCA – Pure red cell aplasia. (See "Acquired pure red cell aplasia in adults".)

Partially treated anemia – Anemia in process of correction or following transfusion. A "dimorphic RBC population" (presence of two distinct populations of RBCs of different sizes) may be suspected when an increased RDW is present; it can be confirmed by examination of the peripheral blood smear, although the distinct populations may not always be recognized. This finding is traditionally taught as a clue to sideroblastic anemia [43]. However, it is more commonly seen during early treatment of iron deficiency or megaloblastic anemia, or following transfusion of a patient with microcytic or macrocytic anemia

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of adrenal insufficiency in adults", section on 'Hematologic findings'.) •Cancer – Cancer-associated anemia, including monoclonal gammopathies. (See "Causes of anemia in patients with cancer".) <span>•Clonal hematopoietic stem cell disorders – Anemia due to a clonal disorder of erythropoiesis (myelodysplastic syndrome, aplastic anemia, or clonal cytopenias of uncertain significance [CCUS]) [42]. The strict definition of clonal hematopoiesis of indeterminate potential (CHIP) includes normal hemoglobin and other blood counts. (See "Clinical manifestations and diagnosis of myelodysplastic syndromes (MDS)" and "Idiopathic and clonal cytopenias of uncertain significance (ICUS and CCUS)".) •Early blood loss – Blood loss that has not yet caused iron deficiency. (See "Evaluation of occult gastrointestinal bleeding".) •PRCA – Pure red cell aplasia. (See "Acquired pure red cell aplasia in adults".) •Partially treated anemia – Anemia in process of correction or following transfusion. A "dimorphic RBC population" (presence of two distinct populations of RBCs of different sizes) may be suspected when an increased RDW is present; it can be confirmed by examination of the peripheral blood smear, although the distinct populations may not always be recognized. This finding is traditionally taught as a clue to sideroblastic anemia [43]. However, it is more commonly seen during early treatment of iron deficiency or megaloblastic anemia, or following transfusion of a patient with microcytic or macrocytic anemia. ●Evaluation •Reticulocyte count and chemistry panel – All individuals with normocytic anemia of unknown cause should have a reticulocyte count and chemistry panel (or review of results




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Reticulocyte count and chemistry panel – All individuals with normocytic anemia of unknown cause should have a reticulocyte count and chemistry panel (or review of results of this testing) during the initial evaluation, and abnormalities of this testing should be pursued (algorithm 1).
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3]. However, it is more commonly seen during early treatment of iron deficiency or megaloblastic anemia, or following transfusion of a patient with microcytic or macrocytic anemia. ●Evaluation •<span>Reticulocyte count and chemistry panel – All individuals with normocytic anemia of unknown cause should have a reticulocyte count and chemistry panel (or review of results of this testing) during the initial evaluation, and abnormalities of this testing should be pursued (algorithm 1). (See 'Laboratory test results' above.) •Iron studies and hemolysis labs – If the reticulocyte count and chemistry panel are unrevealing, determine serum iron concentration, serum TIBC/t




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Iron studies and hemolysis labs – If the reticulocyte count and chemistry panel are unrevealing, determine serum iron concentration, serum TIBC/transferrin, and serum ferritin concentration measured and transferrin saturation (TSAT) calculated, in order to diagnose iron deficiency or ACD/AI. (See "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults".)

If iron stores are normal, evaluate for hemolysis.

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d chemistry panel (or review of results of this testing) during the initial evaluation, and abnormalities of this testing should be pursued (algorithm 1). (See 'Laboratory test results' above.) <span>•Iron studies and hemolysis labs – If the reticulocyte count and chemistry panel are unrevealing, determine serum iron concentration, serum TIBC/transferrin, and serum ferritin concentration measured and transferrin saturation (TSAT) calculated, in order to diagnose iron deficiency or ACD/AI. (See "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults".) If iron stores are normal, evaluate for hemolysis. (See 'Hemolysis' above.) •Additional tests – If hemolysis is absent and there are no other obvious diagnoses, consider conditions listed above including cancer, endocrine disorders, blo




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Additional tests – If hemolysis is absent and there are no other obvious diagnoses, consider conditions listed above including cancer, endocrine disorders, blood loss, and nutrient deficiencies.

- Normocytic anemia with estimated glomerular filtration rate (eGFR) <45 mL/min/1.73 sq m and no other identified cause is most probably the anemia of chronic kidney disease. (See "Overview of the management of chronic kidney disease in adults", section on 'Anemia'.)

- Evaluation for disorders common in older adults is generally reasonable, including testing for monoclonal gammopathies, clonal cytopenias, androgen deficiency (in men), and bone marrow evaluation for myelodysplasia and pure red cell aplasia.

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nose iron deficiency or ACD/AI. (See "Causes and diagnosis of iron deficiency and iron deficiency anemia in adults".) If iron stores are normal, evaluate for hemolysis. (See 'Hemolysis' above.) <span>•Additional tests – If hemolysis is absent and there are no other obvious diagnoses, consider conditions listed above including cancer, endocrine disorders, blood loss, and nutrient deficiencies. -Normocytic anemia with estimated glomerular filtration rate (eGFR) <45 mL/min/1.73 sq m and no other identified cause is most probably the anemia of chronic kidney disease. (See "Overview of the management of chronic kidney disease in adults", section on 'Anemia'.) -Evaluation for disorders common in older adults is generally reasonable, including testing for monoclonal gammopathies, clonal cytopenias, androgen deficiency (in men), and bone marrow evaluation for myelodysplasia and pure red cell aplasia. (See 'Older adults' above.) SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately.




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Poisoning – A number of toxins can cause derangements in respiratory function, leading to dyspnea. Organophosphate poisoning causes an increase in airway secretions and bronchospasm. Petroleum distillates and paraquat can cause respiratory difficulty. Botulism may cause generalized descending muscle weakness involving the respiratory muscles.
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nd "Clinical manifestations of myasthenia gravis" and "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease".) Life-threatening toxic and metabolic causes ●<span>Poisoning – A number of toxins can cause derangements in respiratory function, leading to dyspnea. Organophosphate poisoning causes an increase in airway secretions and bronchospasm. Petroleum distillates and paraquat can cause respiratory difficulty. Botulism may cause generalized descending muscle weakness involving the respiratory muscles. (See "Organophosphate and carbamate poisoning" and "Paraquat poisoning" and "Botulism".) ●Salicylate poisoning – Salicylate overdose leads to stimulation of the medullary respiratory ce




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Salicylate poisoning – Salicylate overdose leads to stimulation of the medullary respiratory center, initially causing hyperventilation and respiratory alkalosis followed by metabolic acidosis. In some cases, pulmonary edema may occur with severe poisoning. Prominent extrapulmonary signs include fever, tinnitus, vertigo, vomiting, diarrhea, and, in more severe cases, mental status changes.
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ifficulty. Botulism may cause generalized descending muscle weakness involving the respiratory muscles. (See "Organophosphate and carbamate poisoning" and "Paraquat poisoning" and "Botulism".) ●<span>Salicylate poisoning – Salicylate overdose leads to stimulation of the medullary respiratory center, initially causing hyperventilation and respiratory alkalosis followed by metabolic acidosis. In some cases, pulmonary edema may occur with severe poisoning. Prominent extrapulmonary signs include fever, tinnitus, vertigo, vomiting, diarrhea, and, in more severe cases, mental status changes. (See "Salicylate (aspirin) poisoning in adults".) ●Carbon monoxide poisoning – Carbon monoxide is a potentially lethal toxin that impairs oxygen transport. Carbon monoxide poisoning may




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Carbon monoxide poisoning – Carbon monoxide is a potentially lethal toxin that impairs oxygen transport. Carbon monoxide poisoning may present with tachypnea and acute dyspnea in moderate cases and pulmonary edema in severe cases. Extrapulmonary signs are generally more prominent and often nonspecific. They can include headache, malaise, chest discomfort, and altered mental status. Pulse oximetry readings are unaffected.
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soning. Prominent extrapulmonary signs include fever, tinnitus, vertigo, vomiting, diarrhea, and, in more severe cases, mental status changes. (See "Salicylate (aspirin) poisoning in adults".) ●<span>Carbon monoxide poisoning – Carbon monoxide is a potentially lethal toxin that impairs oxygen transport. Carbon monoxide poisoning may present with tachypnea and acute dyspnea in moderate cases and pulmonary edema in severe cases. Extrapulmonary signs are generally more prominent and often nonspecific. They can include headache, malaise, chest discomfort, and altered mental status. Pulse oximetry readings are unaffected. (See "Carbon monoxide poisoning".) ●Toxin-related metabolic acidosis – Toxic ingestions, including methanol and ethylene glycol, may cause a metabolic acidosis and compensatory tachypne




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Toxin-related metabolic acidosis – Toxic ingestions, including methanol and ethylene glycol, may cause a metabolic acidosis and compensatory tachypnea that manifest as respiratory distress and may lead to respiratory failure.
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ore prominent and often nonspecific. They can include headache, malaise, chest discomfort, and altered mental status. Pulse oximetry readings are unaffected. (See "Carbon monoxide poisoning".) ●<span>Toxin-related metabolic acidosis – Toxic ingestions, including methanol and ethylene glycol, may cause a metabolic acidosis and compensatory tachypnea that manifest as respiratory distress and may lead to respiratory failure. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".) ●Diabetic ketoacidosis – Diabetic ketoacidosis can cause tachypnea and dyspnea larg




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Diabetic ketoacidosis – Diabetic ketoacidosis can cause tachypnea and dyspnea largely from the body's attempt to correct the metabolic acidosis. Patients with diabetic ketoacidosis may give a history of polyuria, polydipsia, polyphagia, and progressive weakness; signs of severe disease include hyperventilation, altered mental status, abdominal pain, and vomiting
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atory tachypnea that manifest as respiratory distress and may lead to respiratory failure. (See "Methanol and ethylene glycol poisoning: Pharmacology, clinical manifestations, and diagnosis".) ●<span>Diabetic ketoacidosis – Diabetic ketoacidosis can cause tachypnea and dyspnea largely from the body's attempt to correct the metabolic acidosis. Patients with diabetic ketoacidosis may give a history of polyuria, polydipsia, polyphagia, and progressive weakness; signs of severe disease include hyperventilation, altered mental status, abdominal pain, and vomiting. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) ●Sepsis – Severe sepsis often causes respiratory compromise




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Sepsis – Severe sepsis often causes respiratory compromise secondary to tachypnea and respiratory fatigue, which may stem from underlying pneumonia, compensation for lactic acidosis, or some other process.
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perventilation, altered mental status, abdominal pain, and vomiting. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) ●<span>Sepsis – Severe sepsis often causes respiratory compromise secondary to tachypnea and respiratory fatigue, which may stem from underlying pneumonia, compensation for lactic acidosis, or some other process. (See "Evaluation and management of suspected sepsis and septic shock in adults".) ●Anemia – Acute anemia from hemorrhage, hemolysis, or production abnormalities may result in dyspnea du




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Anemia – Acute anemia from hemorrhage, hemolysis, or production abnormalities may result in dyspnea due to the lack of oxygen-carrying capacity
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ry fatigue, which may stem from underlying pneumonia, compensation for lactic acidosis, or some other process. (See "Evaluation and management of suspected sepsis and septic shock in adults".) ●<span>Anemia – Acute anemia from hemorrhage, hemolysis, or production abnormalities may result in dyspnea due to the lack of oxygen-carrying capacity. (See "Diagnostic approach to anemia in adults".) ●Acute chest syndrome – Acute chest syndrome is a potentially life-threatening complication of sickle cell disease. In the United State




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Acute chest syndrome – Acute chest syndrome is a potentially life-threatening complication of sickle cell disease. In the United States, it is seen predominantly in the African-American population. Patients generally complain of severe chest pain and acute dyspnea and have a fever; plain chest radiograph may reveal a new pulmonary infiltrate. It is easily confused with pneumonia but should be considered in any patient with sickle cell disease.
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nemia – Acute anemia from hemorrhage, hemolysis, or production abnormalities may result in dyspnea due to the lack of oxygen-carrying capacity. (See "Diagnostic approach to anemia in adults".) ●<span>Acute chest syndrome – Acute chest syndrome is a potentially life-threatening complication of sickle cell disease. In the United States, it is seen predominantly in the African-American population. Patients generally complain of severe chest pain and acute dyspnea and have a fever; plain chest radiograph may reveal a new pulmonary infiltrate. It is easily confused with pneumonia but should be considered in any patient with sickle cell disease. (See "Overview of the clinical manifestations of sickle cell disease" and "Overview of the pulmonary complications of sickle cell disease".) Miscellaneous causes ●Lung cancer – Shortnes




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Lung cancer – Shortness of breath is a common symptom in patients with lung cancer at the time of diagnosis, occurring in approximately 25 percent of cases. Dyspnea may be due to extrinsic or intraluminal airway obstruction, obstructive pneumonitis or atelectasis, lymphangitic tumor spread, tumor emboli, pneumothorax, pleural effusion, or pericardial effusion with tamponade
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ient with sickle cell disease. (See "Overview of the clinical manifestations of sickle cell disease" and "Overview of the pulmonary complications of sickle cell disease".) Miscellaneous causes ●<span>Lung cancer – Shortness of breath is a common symptom in patients with lung cancer at the time of diagnosis, occurring in approximately 25 percent of cases. Dyspnea may be due to extrinsic or intraluminal airway obstruction, obstructive pneumonitis or atelectasis, lymphangitic tumor spread, tumor emboli, pneumothorax, pleural effusion, or pericardial effusion with tamponade. (See "Clinical manifestations of lung cancer".) ●Pleural effusion – A pleural effusion, secondary to infection, ascites, pancreatitis, cancer, heart failure, pneumonia, or trauma, can




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Pleural effusion – A pleural effusion, secondary to infection, ascites, pancreatitis, cancer, heart failure, pneumonia, or trauma, can cause severe acute dyspnea. Analysis of the pleural fluid is often necessary to determine the source.
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ive pneumonitis or atelectasis, lymphangitic tumor spread, tumor emboli, pneumothorax, pleural effusion, or pericardial effusion with tamponade. (See "Clinical manifestations of lung cancer".) ●<span>Pleural effusion – A pleural effusion, secondary to infection, ascites, pancreatitis, cancer, heart failure, pneumonia, or trauma, can cause severe acute dyspnea. Analysis of the pleural fluid is often necessary to determine the source. (See "Diagnostic evaluation of a pleural effusion in adults: Initial testing".) ●Intraabdominal processes – A number of conditions such as peritonitis, ruptured viscous, or bowel obstru




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Intraabdominal processes – A number of conditions such as peritonitis, ruptured viscous, or bowel obstruction can cause severe pain that affects respiration and may manifest as acute shortness of breath, although this is generally not the patient's primary complaint [12].
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rauma, can cause severe acute dyspnea. Analysis of the pleural fluid is often necessary to determine the source. (See "Diagnostic evaluation of a pleural effusion in adults: Initial testing".) ●<span>Intraabdominal processes – A number of conditions such as peritonitis, ruptured viscous, or bowel obstruction can cause severe pain that affects respiration and may manifest as acute shortness of breath, although this is generally not the patient's primary complaint [12]. (See "Evaluation of the adult with abdominal pain in the emergency department".) ●Ascites – Ascites secondary to malignancy or liver disease can distend the abdominal cavity, placing pr




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Ascites – Ascites secondary to malignancy or liver disease can distend the abdominal cavity, placing pressure on the diaphragm and thereby increasing the work of breathing [13]. In such cases, dyspnea often improves after large-volume paracentesis.
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may manifest as acute shortness of breath, although this is generally not the patient's primary complaint [12]. (See "Evaluation of the adult with abdominal pain in the emergency department".) ●<span>Ascites – Ascites secondary to malignancy or liver disease can distend the abdominal cavity, placing pressure on the diaphragm and thereby increasing the work of breathing [13]. In such cases, dyspnea often improves after large-volume paracentesis. (See "Evaluation of adults with ascites".) ●Pregnancy – A number of physiologic changes occur during pregnancy that affect respiratory function, including an increase in minute ventilat




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Pregnancy – A number of physiologic changes occur during pregnancy that affect respiratory function, including an increase in minute ventilation, a decrease in functional residual capacity, a decrease in hematocrit, and elevation of the diaphragm. Approximately two-thirds of women experience dyspnea during the course of normal pregnancy
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g pressure on the diaphragm and thereby increasing the work of breathing [13]. In such cases, dyspnea often improves after large-volume paracentesis. (See "Evaluation of adults with ascites".) ●<span>Pregnancy – A number of physiologic changes occur during pregnancy that affect respiratory function, including an increase in minute ventilation, a decrease in functional residual capacity, a decrease in hematocrit, and elevation of the diaphragm. Approximately two-thirds of women experience dyspnea during the course of normal pregnancy. However, pregnancy increases the risk for several potentially life-threatening conditions that may manifest with dyspnea, notably PE. Pulmonary edema may be identified in the setting o




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Massive obesity – Massive abdominal girth can interfere with ventilation, causing dyspnea and hypoxia.
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diagnosis" and "Eclampsia" and "Amniotic fluid embolism" and "Peripartum cardiomyopathy: Etiology, clinical manifestations, and diagnosis" and "Management of heart failure during pregnancy".) ●<span>Massive obesity – Massive abdominal girth can interfere with ventilation, causing dyspnea and hypoxia. (See "Epidemiology and pathogenesis of obesity hypoventilation syndrome" and "Overweight and obesity in adults: Health consequences".) ●Hyperventilation and anxiety – Hyperventilation f




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Hyperventilation and anxiety – Hyperventilation from anxiety is a diagnosis of exclusion in the ED. Even among young, healthy patients with a known anxiety disorder, it is prudent to perform a history and physical examination to screen for medical causes of dyspnea. To complicate matters, anxiety is common among patients with severe medical disease. As an example, COPD patients have a threefold increase in the prevalence of anxiety disorders compared with the general population [14]
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interfere with ventilation, causing dyspnea and hypoxia. (See "Epidemiology and pathogenesis of obesity hypoventilation syndrome" and "Overweight and obesity in adults: Health consequences".) ●<span>Hyperventilation and anxiety – Hyperventilation from anxiety is a diagnosis of exclusion in the ED. Even among young, healthy patients with a known anxiety disorder, it is prudent to perform a history and physical examination to screen for medical causes of dyspnea. To complicate matters, anxiety is common among patients with severe medical disease. As an example, COPD patients have a threefold increase in the prevalence of anxiety disorders compared with the general population [14]. In such patients, it is best to assume that an exacerbation of their underlying medical disease is the cause of dyspnea until proven otherwise. HISTORY — The history is critical to the




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If it resembles prior episodes, the current problem is often an exacerbation of a preexisting illness. The medical record and medication list can provide important diagnostic clues
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t preexisting medical conditions, such as asthma, chronic obstructive pulmonary disease (COPD), or ischemic heart disease, and whether the patient has experienced similar acute episodes before. <span>If it resembles prior episodes, the current problem is often an exacerbation of a preexisting illness. The medical record and medication list can provide important diagnostic clues. ●Prior intubation – Patients with a history of endotracheal intubation for medical conditions have a higher risk for severe disease and the need for subsequent intubation. As an exampl




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Prior intubation – Patients with a history of endotracheal intubation for medical conditions have a higher risk for severe disease and the need for subsequent intubation. As an example, patients who have required intubation for a severe asthma exacerbation are at increased risk for subsequent episodes of near-fatal asthma attacks.
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es before. If it resembles prior episodes, the current problem is often an exacerbation of a preexisting illness. The medical record and medication list can provide important diagnostic clues. ●<span>Prior intubation – Patients with a history of endotracheal intubation for medical conditions have a higher risk for severe disease and the need for subsequent intubation. As an example, patients who have required intubation for a severe asthma exacerbation are at increased risk for subsequent episodes of near-fatal asthma attacks. (See "Identifying patients at risk for fatal asthma".) ●Time course – Ask whether the dyspnea developed suddenly or gradually. Keep in mind that exacerbations of a single illness can pr




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Time course – Ask whether the dyspnea developed suddenly or gradually. Keep in mind that exacerbations of a single illness can present in different ways and over different periods of time. As examples, an asthma flare may develop over minutes or days, as may episodes of heart failure. Both may cause acute exacerbations of dyspnea as well. A table is provided to help differentiate causes of respiratory distress based on time course (table 2)
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who have required intubation for a severe asthma exacerbation are at increased risk for subsequent episodes of near-fatal asthma attacks. (See "Identifying patients at risk for fatal asthma".) ●<span>Time course – Ask whether the dyspnea developed suddenly or gradually. Keep in mind that exacerbations of a single illness can present in different ways and over different periods of time. As examples, an asthma flare may develop over minutes or days, as may episodes of heart failure. Both may cause acute exacerbations of dyspnea as well. A table is provided to help differentiate causes of respiratory distress based on time course (table 2). ●Severity – Ask how severe (mild, moderate, high) the dyspnea is compared with their baseline. It is important to distinguish an acute presentation from an acute on chronic presentatio




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Severity – Ask how severe (mild, moderate, high) the dyspnea is compared with their baseline. It is important to distinguish an acute presentation from an acute on chronic presentation.
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s may episodes of heart failure. Both may cause acute exacerbations of dyspnea as well. A table is provided to help differentiate causes of respiratory distress based on time course (table 2). ●<span>Severity – Ask how severe (mild, moderate, high) the dyspnea is compared with their baseline. It is important to distinguish an acute presentation from an acute on chronic presentation. ●Chest pain – Chest pain in association with dyspnea occurs with a number of diseases, including acute coronary syndrome (ACS), pneumothorax, and PE. Of note, a sizable minority of pati




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Chest pain – Chest pain in association with dyspnea occurs with a number of diseases, including acute coronary syndrome (ACS), pneumothorax, and PE. Of note, a sizable minority of patients with ACS or PE complain of dyspnea alone
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e 2). ●Severity – Ask how severe (mild, moderate, high) the dyspnea is compared with their baseline. It is important to distinguish an acute presentation from an acute on chronic presentation. ●<span>Chest pain – Chest pain in association with dyspnea occurs with a number of diseases, including acute coronary syndrome (ACS), pneumothorax, and PE. Of note, a sizable minority of patients with ACS or PE complain of dyspnea alone. (See "Evaluation of the adult with chest pain in the emergency department".) ●Trauma – Injury to the airway, neck, chest wall, lungs, heart, mediastinal structures, or abdomen can lead




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Trauma – Injury to the airway, neck, chest wall, lungs, heart, mediastinal structures, or abdomen can lead to dyspnea. Acute symptoms may not manifest until a day or longer following trauma.
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rome (ACS), pneumothorax, and PE. Of note, a sizable minority of patients with ACS or PE complain of dyspnea alone. (See "Evaluation of the adult with chest pain in the emergency department".) ●<span>Trauma – Injury to the airway, neck, chest wall, lungs, heart, mediastinal structures, or abdomen can lead to dyspnea. Acute symptoms may not manifest until a day or longer following trauma. (See "Initial evaluation and management of blunt thoracic trauma in adults".) ●Fever – Fever can be associated with an infection, hypersensitivity pneumonitis, aspiration pneumonitis, o




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Fever – Fever can be associated with an infection, hypersensitivity pneumonitis, aspiration pneumonitis, or poisoning. As an example of the latter, aspirin overdose can present with fever and abnormal breathing.
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tructures, or abdomen can lead to dyspnea. Acute symptoms may not manifest until a day or longer following trauma. (See "Initial evaluation and management of blunt thoracic trauma in adults".) ●<span>Fever – Fever can be associated with an infection, hypersensitivity pneumonitis, aspiration pneumonitis, or poisoning. As an example of the latter, aspirin overdose can present with fever and abnormal breathing. (See "Salicylate (aspirin) poisoning in adults".) ●Paroxysmal nocturnal dyspnea (PND) – Keep in mind that PND is not specific for ADHF. Patients with COPD may present with a similar his




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Paroxysmal nocturnal dyspnea (PND) – Keep in mind that PND is not specific for ADHF. Patients with COPD may present with a similar history.
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neumonitis, aspiration pneumonitis, or poisoning. As an example of the latter, aspirin overdose can present with fever and abnormal breathing. (See "Salicylate (aspirin) poisoning in adults".) ●<span>Paroxysmal nocturnal dyspnea (PND) – Keep in mind that PND is not specific for ADHF. Patients with COPD may present with a similar history. ●Hemoptysis – Hemoptysis is associated with a number of conditions, including severe valvular disease (eg, mitral stenosis), PE, tuberculosis, malignancy when tumors erode into a vascul




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Cough and sputum – The presence and quality of sputum may be helpful. Purulent sputum suggests pneumonia and white or pink frothy sputum suggests ADHF, while frankly bloody sputum suggests infection (eg, tuberculosis) or pulmonary hemorrhage (eg, PE or malignancy). A nonproductive cough is a nonspecific symptom and may be associated with asthma, heart failure, respiratory infection, or PE
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mitral stenosis), PE, tuberculosis, malignancy when tumors erode into a vascular structure, and the effects of anticoagulants. (See "Evaluation and management of life-threatening hemoptysis".) ●<span>Cough and sputum – The presence and quality of sputum may be helpful. Purulent sputum suggests pneumonia and white or pink frothy sputum suggests ADHF, while frankly bloody sputum suggests infection (eg, tuberculosis) or pulmonary hemorrhage (eg, PE or malignancy). A nonproductive cough is a nonspecific symptom and may be associated with asthma, heart failure, respiratory infection, or PE. ●Medications – A review of the patient's medications can prove helpful. In addition to information about chronic or acute illness (eg, recent antibiotic prescription), a medication lis




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Hemoptysis – Hemoptysis is associated with a number of conditions, including severe valvular disease (eg, mitral stenosis), PE, tuberculosis, malignancy when tumors erode into a vascular structure, and the effects of anticoagulants.
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. (See "Salicylate (aspirin) poisoning in adults".) ●Paroxysmal nocturnal dyspnea (PND) – Keep in mind that PND is not specific for ADHF. Patients with COPD may present with a similar history. ●<span>Hemoptysis – Hemoptysis is associated with a number of conditions, including severe valvular disease (eg, mitral stenosis), PE, tuberculosis, malignancy when tumors erode into a vascular structure, and the effects of anticoagulants. (See "Evaluation and management of life-threatening hemoptysis".) ●Cough and sputum – The presence and quality of sputum may be helpful. Purulent sputum suggests pneumonia and white or




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Medications – A review of the patient's medications can prove helpful. In addition to information about chronic or acute illness (eg, recent antibiotic prescription), a medication list may provide information about recent changes in medications or dosing. It is important to ask about compliance. Obtaining information directly from the patient's pharmacy can be helpful
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eg, tuberculosis) or pulmonary hemorrhage (eg, PE or malignancy). A nonproductive cough is a nonspecific symptom and may be associated with asthma, heart failure, respiratory infection, or PE. ●<span>Medications – A review of the patient's medications can prove helpful. In addition to information about chronic or acute illness (eg, recent antibiotic prescription), a medication list may provide information about recent changes in medications or dosing. It is important to ask about compliance. Obtaining information directly from the patient's pharmacy can be helpful. ●Tobacco and drugs – Knowledge of the patient's tobacco and drug use can provide insight into the differential diagnosis. Tobacco use increases the risk for a number of chronic conditi




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Tobacco and drugs – Knowledge of the patient's tobacco and drug use can provide insight into the differential diagnosis. Tobacco use increases the risk for a number of chronic conditions (eg, COPD, malignancy), while inhaled drug use can lead to such conditions as crack lung and acute respiratory distress syndrome (ARDS). Noninhalational use or overdose of certain drugs such as opioids and aspirin can produce acute lung injury
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list may provide information about recent changes in medications or dosing. It is important to ask about compliance. Obtaining information directly from the patient's pharmacy can be helpful. ●<span>Tobacco and drugs – Knowledge of the patient's tobacco and drug use can provide insight into the differential diagnosis. Tobacco use increases the risk for a number of chronic conditions (eg, COPD, malignancy), while inhaled drug use can lead to such conditions as crack lung and acute respiratory distress syndrome (ARDS). Noninhalational use or overdose of certain drugs such as opioids and aspirin can produce acute lung injury. (See "Cocaine: Acute intoxication" and "Acute opioid intoxication in adults" and "Salicylate (aspirin) poisoning in adults" and "Overview of pulmonary disease in people who inject drug




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Psychiatric conditions – Psychogenic causes for acute dyspnea represent diagnoses of exclusion in the emergency department (ED). Organic causes must be thoroughly considered first. Nevertheless, among patients younger than 40 years with no medical conditions, psychogenic dyspnea (eg, anxiety attack) may be the cause in a sizable minority of patients [15,16]
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n adults" and "Salicylate (aspirin) poisoning in adults" and "Overview of pulmonary disease in people who inject drugs" and "E-cigarette or vaping product use associated lung injury (EVALI)".) ●<span>Psychiatric conditions – Psychogenic causes for acute dyspnea represent diagnoses of exclusion in the emergency department (ED). Organic causes must be thoroughly considered first. Nevertheless, among patients younger than 40 years with no medical conditions, psychogenic dyspnea (eg, anxiety attack) may be the cause in a sizable minority of patients [15,16]. PHYSICAL EXAMINATION Clinical danger signs — The clinician should perform a screening physical examination looking for signs of significant respiratory distress in all patients with ac




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Signs that portend imminent respiratory arrest include:

● Depressed mental status

● Inability to maintain respiratory effort

● Cyanosis

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hould perform a screening physical examination looking for signs of significant respiratory distress in all patients with acute dyspnea. A brief inspection is often sufficient for this purpose. <span>Signs that portend imminent respiratory arrest include: ●Depressed mental status ●Inability to maintain respiratory effort ●Cyanosis Many patients in respiratory distress appear anxious and sit bolt upright or in a tripod position. They often breathe rapidly, use accessory muscles, and sweat profusely. They may be un




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Signs suggestive of severe respiratory distress include:

● Retractions and the use of accessory muscles

● Brief, fragmented speech

● Inability to lie supine (an exception is hepatopulmonary syndrome where patients may breathe more comfortably when recumbent) (See "Hepatopulmonary syndrome in adults: Prevalence, causes, clinical manifestations, and diagnosis", section on 'Dyspnea'.)

● Profound diaphoresis; dusky skin

● Agitation or other altered mental status

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er questions with anything more than a few words. Stridor or wheezing may be audible. However, patients with a depressed mental status from CO2 retention may look comfortable and lackadaisical. <span>Signs suggestive of severe respiratory distress include: ●Retractions and the use of accessory muscles ●Brief, fragmented speech ●Inability to lie supine (an exception is hepatopulmonary syndrome where patients may breathe more comfortably when recumbent) (See "Hepatopulmonary syndrome in adults: Prevalence, causes, clinical manifestations, and diagnosis", section on 'Dyspnea'.) ●Profound diaphoresis; dusky skin ●Agitation or other altered mental status Retractions occur with airway obstruction (eg, asthma, chronic obstructive pulmonary disease [COPD], foreign body) and can be seen in the suprasternal, intercostal, and subcostal areas




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Retractions occur with airway obstruction (eg, asthma, chronic obstructive pulmonary disease [COPD], foreign body) and can be seen in the suprasternal, intercostal, and subcostal areas [17]. They are an ominous sign suggesting extreme respiratory distress. The use of accessory muscles to breathe suggests fatigue of the respiratory muscles and the potential for respiratory failure. Remember that those with neuromuscular disease may not manifest retractions due to muscle weakness, even in the face of severe pulmonary compromise.

Diaphoresis reflects extreme sympathetic stimulation associated with severe disease (eg, myocardial infarction, severe asthma flare). Cyanosis is uncommon and indicates severe hypoxia or methemoglobinemia.

Altered mental status (eg, agitation or somnolence) in the dyspneic patient suggests severe hypoxia or hypercarbia. It may also be caused by a toxin (eg, salicylate overdose, carbon monoxide) or underlying pathology (eg, hypoglycemia, sepsis)

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patopulmonary syndrome in adults: Prevalence, causes, clinical manifestations, and diagnosis", section on 'Dyspnea'.) ●Profound diaphoresis; dusky skin ●Agitation or other altered mental status <span>Retractions occur with airway obstruction (eg, asthma, chronic obstructive pulmonary disease [COPD], foreign body) and can be seen in the suprasternal, intercostal, and subcostal areas [17]. They are an ominous sign suggesting extreme respiratory distress. The use of accessory muscles to breathe suggests fatigue of the respiratory muscles and the potential for respiratory failure. Remember that those with neuromuscular disease may not manifest retractions due to muscle weakness, even in the face of severe pulmonary compromise. Diaphoresis reflects extreme sympathetic stimulation associated with severe disease (eg, myocardial infarction, severe asthma flare). Cyanosis is uncommon and indicates severe hypoxia or methemoglobinemia. Altered mental status (eg, agitation or somnolence) in the dyspneic patient suggests severe hypoxia or hypercarbia. It may also be caused by a toxin (eg, salicylate overdose, carbon monoxide) or underlying pathology (eg, hypoglycemia, sepsis). General examination findings — Once a screen for clinical danger signs is completed and any necessary resuscitation is initiated, a more thorough physical examination is performed. Imp




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General examination findings — Once a screen for clinical danger signs is completed and any necessary resuscitation is initiated, a more thorough physical examination is performed. Important items to note are described below and in the accompanying table (table 3). Keep in mind that an unremarkable pulmonary and cardiac examination does not rule out significant disease. As examples, the sensitivity and specificity of the pulmonary examination are limited for making the diagnosis of pneumonia or acute decompensated heart failure (ADHF) [18-22]
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) in the dyspneic patient suggests severe hypoxia or hypercarbia. It may also be caused by a toxin (eg, salicylate overdose, carbon monoxide) or underlying pathology (eg, hypoglycemia, sepsis). <span>General examination findings — Once a screen for clinical danger signs is completed and any necessary resuscitation is initiated, a more thorough physical examination is performed. Important items to note are described below and in the accompanying table (table 3). Keep in mind that an unremarkable pulmonary and cardiac examination does not rule out significant disease. As examples, the sensitivity and specificity of the pulmonary examination are limited for making the diagnosis of pneumonia or acute decompensated heart failure (ADHF) [18-22]. ●Respiratory rate (RR) – Patients with serious underlying disease may have a fast, normal, or slow RR. As an example, patients with a pulmonary embolism (PE) may have a RR in the norma




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● Respiratory rate (RR) – Patients with serious underlying disease may have a fast, normal, or slow RR. As an example, patients with a pulmonary embolism (PE) may have a RR in the normal range. Note that measurements of the RR obtained during triage may not be accurate [23,24].

● Pulse oximetry – Pulse oximetry provides crucial information about arterial oxygenation. However, clinicians must be aware that standard pulse oximeters are not accurate in the setting of hypothermia, shock, carbon monoxide poisoning, and methemoglobinemia.

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ificant disease. As examples, the sensitivity and specificity of the pulmonary examination are limited for making the diagnosis of pneumonia or acute decompensated heart failure (ADHF) [18-22]. <span>●Respiratory rate (RR) – Patients with serious underlying disease may have a fast, normal, or slow RR. As an example, patients with a pulmonary embolism (PE) may have a RR in the normal range. Note that measurements of the RR obtained during triage may not be accurate [23,24]. ●Pulse oximetry – Pulse oximetry provides crucial information about arterial oxygenation. However, clinicians must be aware that standard pulse oximeters are not accurate in the setting of hypothermia, shock, carbon monoxide poisoning, and methemoglobinemia. (See "Pulse oximetry".) In general, healthy individuals demonstrate an oxygen saturation (SpO2) of 95 percent or greater. Older adults and patients who are obese or smoke heavily often




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In general, healthy individuals demonstrate an oxygen saturation (SpO2) of 95 percent or greater. Older adults and patients who are obese or smoke heavily often maintain levels between 92 and 95 percent, while patients with severe chronic lung disease may have baseline levels below 92 percent. In the setting of acute dyspnea, oxygenation levels lower than expected or below a patient's known baseline should be investigated and explained.
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However, clinicians must be aware that standard pulse oximeters are not accurate in the setting of hypothermia, shock, carbon monoxide poisoning, and methemoglobinemia. (See "Pulse oximetry".) <span>In general, healthy individuals demonstrate an oxygen saturation (SpO2) of 95 percent or greater. Older adults and patients who are obese or smoke heavily often maintain levels between 92 and 95 percent, while patients with severe chronic lung disease may have baseline levels below 92 percent. In the setting of acute dyspnea, oxygenation levels lower than expected or below a patient's known baseline should be investigated and explained. A profound drop in SpO2 associated with exercise is characteristic of Pneumocystis pneumonia. SpO2 levels before and after exercise should be noted in patients suspected or known to hav




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A profound drop in SpO2 associated with exercise is characteristic of Pneumocystis pneumonia. SpO2 levels before and after exercise should be noted in patients suspected or known to have HIV.
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ease may have baseline levels below 92 percent. In the setting of acute dyspnea, oxygenation levels lower than expected or below a patient's known baseline should be investigated and explained. <span>A profound drop in SpO2 associated with exercise is characteristic of Pneumocystis pneumonia. SpO2 levels before and after exercise should be noted in patients suspected or known to have HIV. (See "Clinical presentation and diagnosis of Pneumocystis pulmonary infection in patients with HIV".) ●Other vital signs – Clinicians must review a complete set of vital signs. Dyspnea




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Abnormal breath sounds:

• Stridor occurs when there is airway obstruction. Inspiratory stridor suggests obstruction above the vocal cords (eg, foreign body, epiglottitis, angioedema). Expiratory stridor or mixed inspiratory and expiratory stridor suggests obstruction below the vocal cords (eg, croup, bacterial tracheitis, foreign body).

• Wheezing suggests obstruction below the level of the trachea and is found with asthma, anaphylaxis, a foreign body in a mainstem bronchus, ADHF, or a fixed lesion such as a tumor.

• Crackles (rales) suggest the presence of interalveolar fluid, as seen with pneumonia or ADHF. They can also occur with pulmonary fibrosis. However, the absence of crackles does not rule out the presence of pneumonia, ADHF, or pulmonary fibrosis [18].

• Diminished breath sounds can be caused by anything that prevents air from entering the lungs. Such conditions include: severe COPD, severe asthma, pneumothorax, tension pneumothorax, and hemothorax, among others.

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nosis of Pneumocystis pulmonary infection in patients with HIV".) ●Other vital signs – Clinicians must review a complete set of vital signs. Dyspnea and hypotension are an ominous combination. ●<span>Abnormal breath sounds: •Stridor occurs when there is airway obstruction. Inspiratory stridor suggests obstruction above the vocal cords (eg, foreign body, epiglottitis, angioedema). Expiratory stridor or mixed inspiratory and expiratory stridor suggests obstruction below the vocal cords (eg, croup, bacterial tracheitis, foreign body). •Wheezing suggests obstruction below the level of the trachea and is found with asthma, anaphylaxis, a foreign body in a mainstem bronchus, ADHF, or a fixed lesion such as a tumor. •Crackles (rales) suggest the presence of interalveolar fluid, as seen with pneumonia or ADHF. They can also occur with pulmonary fibrosis. However, the absence of crackles does not rule out the presence of pneumonia, ADHF, or pulmonary fibrosis [18]. •Diminished breath sounds can be caused by anything that prevents air from entering the lungs. Such conditions include: severe COPD, severe asthma, pneumothorax, tension pneumothorax, and hemothorax, among others. ●Cardiovascular signs: •An abnormal heart rhythm may be a response to underlying disease (eg, tachycardia in the setting of PE) or the cause of dyspnea (eg, atrial fibrillation in the s




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● Cardiovascular signs:

• An abnormal heart rhythm may be a response to underlying disease (eg, tachycardia in the setting of PE) or the cause of dyspnea (eg, atrial fibrillation in the setting of chronic heart failure).

• Heart murmurs may be present with ADHF or diseased or otherwise compromised cardiac valves. (See "Auscultation of heart sounds".)

• An S3 heart sound suggests left ventricular systolic dysfunction, especially in the setting of ADHF.

• An S4 heart sound suggests left ventricular dysfunction and may be present with severe hypertension, aortic stenosis, hypertrophic cardiomyopathy, ischemic heart disease, or acute mitral regurgitation.

• Muffled or distant heart sounds suggest the presence of cardiac tamponade but must be interpreted in the context of the overall clinical setting.

• Elevated jugular venous pressure may be present with ADHF, cardiac tamponade, or any other cause of elevated intrathoracic pressure that prevents right heart filling. It can be assessed by observing jugular venous distension (picture 1) or examining hepatojugular reflux

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ounds can be caused by anything that prevents air from entering the lungs. Such conditions include: severe COPD, severe asthma, pneumothorax, tension pneumothorax, and hemothorax, among others. <span>●Cardiovascular signs: •An abnormal heart rhythm may be a response to underlying disease (eg, tachycardia in the setting of PE) or the cause of dyspnea (eg, atrial fibrillation in the setting of chronic heart failure). •Heart murmurs may be present with ADHF or diseased or otherwise compromised cardiac valves. (See "Auscultation of heart sounds".) •An S3 heart sound suggests left ventricular systolic dysfunction, especially in the setting of ADHF. •An S4 heart sound suggests left ventricular dysfunction and may be present with severe hypertension, aortic stenosis, hypertrophic cardiomyopathy, ischemic heart disease, or acute mitral regurgitation. •Muffled or distant heart sounds suggest the presence of cardiac tamponade but must be interpreted in the context of the overall clinical setting. •Elevated jugular venous pressure may be present with ADHF, cardiac tamponade, or any other cause of elevated intrathoracic pressure that prevents right heart filling. It can be assessed by observing jugular venous distension (picture 1) or examining hepatojugular reflux. ●Pulsus paradoxus – Pulsus paradoxus can occur when right heart function is compromised such as can be seen with severe asthma, pulmonary embolism, or cardiac tamponade. (See "Pulsus p




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● Pulsus paradoxus – Pulsus paradoxus can occur when right heart function is compromised such as can be seen with severe asthma, pulmonary embolism, or cardiac tamponade. (See "Pulsus paradoxus in pericardial disease".)

Under normal conditions, inspiration increases systemic venous return and right heart volumes increase; the free wall of the right ventricle expands into the unoccupied pericardial space with little impact on left heart volume.

When the pressure within the pericardial sac acutely increases, the effective compliance of all cardiac chambers is limited to that of the tightly stretched pericardium. As a result, the increase in right heart filling that occurs during inspiration can only be accommodated by a bowing of the interventricular septum toward the left heart. This leads to a reduction in left ventricular diastolic volume, a lower stroke volume, and a consequent decrease in systolic pressure during inspiration (waveform 1)

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or any other cause of elevated intrathoracic pressure that prevents right heart filling. It can be assessed by observing jugular venous distension (picture 1) or examining hepatojugular reflux. <span>●Pulsus paradoxus – Pulsus paradoxus can occur when right heart function is compromised such as can be seen with severe asthma, pulmonary embolism, or cardiac tamponade. (See "Pulsus paradoxus in pericardial disease".) Under normal conditions, inspiration increases systemic venous return and right heart volumes increase; the free wall of the right ventricle expands into the unoccupied pericardial space with little impact on left heart volume. When the pressure within the pericardial sac acutely increases, the effective compliance of all cardiac chambers is limited to that of the tightly stretched pericardium. As a result, the increase in right heart filling that occurs during inspiration can only be accommodated by a bowing of the interventricular septum toward the left heart. This leads to a reduction in left ventricular diastolic volume, a lower stroke volume, and a consequent decrease in systolic pressure during inspiration (waveform 1). In order to determine if a pulsus paradoxus is present, measure the patient's systolic blood pressure after a normal exhalation. Then have the patient inhale normally and determine sys




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In order to determine if a pulsus paradoxus is present, measure the patient's systolic blood pressure after a normal exhalation. Then have the patient inhale normally and determine systolic pressure when the lungs are expanded. Pulsus paradoxus exists if the difference in systolic pressures is greater than 10 mmHg. Keep in mind that the absence of pulsus paradoxus does not rule out any disease.
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tum toward the left heart. This leads to a reduction in left ventricular diastolic volume, a lower stroke volume, and a consequent decrease in systolic pressure during inspiration (waveform 1). <span>In order to determine if a pulsus paradoxus is present, measure the patient's systolic blood pressure after a normal exhalation. Then have the patient inhale normally and determine systolic pressure when the lungs are expanded. Pulsus paradoxus exists if the difference in systolic pressures is greater than 10 mmHg. Keep in mind that the absence of pulsus paradoxus does not rule out any disease. ●Inspection – Examine the skin for discoloration suggesting hypoxia or poor perfusion, signs of an allergic reaction, and evidence of trauma. ●Extremities – Peripheral edema may not occ




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● Inspection – Examine the skin for discoloration suggesting hypoxia or poor perfusion, signs of an allergic reaction, and evidence of trauma.

● Extremities – Peripheral edema may not occur with acute left heart failure, but if present suggests ADHF as the cause of dyspnea. Clubbing is associated with conditions causing chronic hypoxemia.

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the lungs are expanded. Pulsus paradoxus exists if the difference in systolic pressures is greater than 10 mmHg. Keep in mind that the absence of pulsus paradoxus does not rule out any disease. <span>●Inspection – Examine the skin for discoloration suggesting hypoxia or poor perfusion, signs of an allergic reaction, and evidence of trauma. ●Extremities – Peripheral edema may not occur with acute left heart failure, but if present suggests ADHF as the cause of dyspnea. Clubbing is associated with conditions causing chronic hypoxemia. ANCILLARY STUDIES General approach — Ancillary testing should be performed in the context of the history and examination findings. Random testing without a clear differential diagnosis




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General approach — Ancillary testing should be performed in the context of the history and examination findings. Random testing without a clear differential diagnosis can mislead the clinician and delay appropriate management. The use of dyspnea biomarker panels does not appear to improve accuracy beyond clinical assessment and focused testing [25,26]. Nevertheless, a plain chest radiograph (CXR) and an electrocardiogram are obtained in most emergency department (ED) patients with acute dyspnea
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eral edema may not occur with acute left heart failure, but if present suggests ADHF as the cause of dyspnea. Clubbing is associated with conditions causing chronic hypoxemia. ANCILLARY STUDIES <span>General approach — Ancillary testing should be performed in the context of the history and examination findings. Random testing without a clear differential diagnosis can mislead the clinician and delay appropriate management. The use of dyspnea biomarker panels does not appear to improve accuracy beyond clinical assessment and focused testing [25,26]. Nevertheless, a plain chest radiograph (CXR) and an electrocardiogram are obtained in most emergency department (ED) patients with acute dyspnea. Plain chest radiograph (CXR) — A CXR is obtained for most ED patients with acute dyspnea (an exception being otherwise asymptomatic asthma patients who respond well to treatment). When




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● Acute heart failure – Signs of acute decompensated heart failure (ADHF) that may appear on a CXR include: cardiomegaly, cephalization of blood vessels, interstitial edema (eg, "Kerley B" lines, peribronchial cuffing), and vascular congestion (image 1). Pleural effusions may be present. Keep in mind that the radiograph may lag behind the clinical picture and approximately 20 percent of patients admitted with ADHF have a nondiagnostic CXR [27]. Lung ultrasound is more sensitive than CXR in diagnosing ADHF and should be used if resources are available [28,29].
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ute dyspnea (an exception being otherwise asymptomatic asthma patients who respond well to treatment). When abnormalities are identified, it is useful to compare the radiograph to past studies. <span>●Acute heart failure – Signs of acute decompensated heart failure (ADHF) that may appear on a CXR include: cardiomegaly, cephalization of blood vessels, interstitial edema (eg, "Kerley B" lines, peribronchial cuffing), and vascular congestion (image 1). Pleural effusions may be present. Keep in mind that the radiograph may lag behind the clinical picture and approximately 20 percent of patients admitted with ADHF have a nondiagnostic CXR [27]. Lung ultrasound is more sensitive than CXR in diagnosing ADHF and should be used if resources are available [28,29]. (See "Heart failure: Clinical manifestations and diagnosis in adults".) ●Pneumonia – Although an infiltrate on CXR is considered the "gold standard" for diagnosing pneumonia (image 2),




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● Pneumonia – Although an infiltrate on CXR is considered the "gold standard" for diagnosing pneumonia (image 2), radiographs obtained early in the clinical course may be nondiagnostic [30]. Volume depletion may also lead to a negative initial CXR. Contrary to past teaching, the appearance of the CXR (lobar versus diffuse disease) does not accurately predict the nature of the pneumonia (eg, "typical" versus "atypical" organisms).
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27]. Lung ultrasound is more sensitive than CXR in diagnosing ADHF and should be used if resources are available [28,29]. (See "Heart failure: Clinical manifestations and diagnosis in adults".) <span>●Pneumonia – Although an infiltrate on CXR is considered the "gold standard" for diagnosing pneumonia (image 2), radiographs obtained early in the clinical course may be nondiagnostic [30]. Volume depletion may also lead to a negative initial CXR. Contrary to past teaching, the appearance of the CXR (lobar versus diffuse disease) does not accurately predict the nature of the pneumonia (eg, "typical" versus "atypical" organisms). (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".) ●Pneumothorax – A pneumothorax sufficient to cause acute dyspnea is usually visible on CXR




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● Pneumothorax – A pneumothorax sufficient to cause acute dyspnea is usually visible on CXR (image 3). An expiratory view may be helpful [31]. Patients in extremis with a suggestive history and examination findings consistent with a tension pneumothorax (eg, hypotension, elevated neck veins, unilateral diminished or absent breath sounds) should be treated with immediate needle decompression before obtaining a CXR.
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es not accurately predict the nature of the pneumonia (eg, "typical" versus "atypical" organisms). (See "Clinical evaluation and diagnostic testing for community-acquired pneumonia in adults".) <span>●Pneumothorax – A pneumothorax sufficient to cause acute dyspnea is usually visible on CXR (image 3). An expiratory view may be helpful [31]. Patients in extremis with a suggestive history and examination findings consistent with a tension pneumothorax (eg, hypotension, elevated neck veins, unilateral diminished or absent breath sounds) should be treated with immediate needle decompression before obtaining a CXR. ●Chronic obstructive pulmonary disease (COPD) and asthma – Large lung volumes and a flattened diaphragm on CXR suggest air trapping, which occurs with COPD (image 4) or asthma. Unilater




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● Chronic obstructive pulmonary disease (COPD) and asthma – Large lung volumes and a flattened diaphragm on CXR suggest air trapping, which occurs with COPD (image 4) or asthma. Unilateral air trapping suggests a foreign body (image 5). Many patients with mildly or moderately severe COPD and most patients with asthma have an unremarkable CXR
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t with a tension pneumothorax (eg, hypotension, elevated neck veins, unilateral diminished or absent breath sounds) should be treated with immediate needle decompression before obtaining a CXR. <span>●Chronic obstructive pulmonary disease (COPD) and asthma – Large lung volumes and a flattened diaphragm on CXR suggest air trapping, which occurs with COPD (image 4) or asthma. Unilateral air trapping suggests a foreign body (image 5). Many patients with mildly or moderately severe COPD and most patients with asthma have an unremarkable CXR. (See "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging" and "Acute exacerbations of asthma in adults: Home and office management".) Ul




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Ultrasound — Ultrasound is an effective tool for investigating several important causes of acute dyspnea including ADHF, pericardial tamponade (movie 1), and clinically significant pneumothorax (image 6), pneumonia, or pleural effusion. In addition, ultrasound can be used to identify cardiac wall motion abnormalities suggestive of ischemia or pulmonary embolism, as well as proximal deep vein thromboses, the presence of which supports the diagnosis of pulmonary embolism in the appropriate clinical setting.
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rkable CXR. (See "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging" and "Acute exacerbations of asthma in adults: Home and office management".) <span>Ultrasound — Ultrasound is an effective tool for investigating several important causes of acute dyspnea including ADHF, pericardial tamponade (movie 1), and clinically significant pneumothorax (image 6), pneumonia, or pleural effusion. In addition, ultrasound can be used to identify cardiac wall motion abnormalities suggestive of ischemia or pulmonary embolism, as well as proximal deep vein thromboses, the presence of which supports the diagnosis of pulmonary embolism in the appropriate clinical setting. (See "Indications for bedside ultrasonography in the critically-ill adult patient" and "Emergency ultrasound in adults with abdominal and thoracic trauma", section on 'Pericardial and l




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Electrocardiogram (ECG) — An ECG with ST segment changes constitutes strong evidence supporting the diagnosis of cardiac ischemia. However, clinicians must remember that neither normal biomarkers nor a nondiagnostic ECG can rule out cardiac disease in the ED. The initial ECG is normal in approximately 20 percent of patients subsequently diagnosed with a myocardial infarction, and only 33 percent of initial ECGs are diagnostic. The ECG may also reveal signs of pulmonary embolism (PE) (right heart strain), pericardial effusion (diffuse low voltage (waveform 2), electrical alternans (waveform 3)), and other disease processes. However, the sensitivity and specificity of the ECG for PE is limited. It is helpful to compare the ECG with prior studies.
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on 'Pleural examination' and "Imaging of pleural effusions in adults", section on 'Ultrasonography' and "Clinical presentation and diagnosis of pneumothorax", section on 'Diagnostic imaging'.) <span>Electrocardiogram (ECG) — An ECG with ST segment changes constitutes strong evidence supporting the diagnosis of cardiac ischemia. However, clinicians must remember that neither normal biomarkers nor a nondiagnostic ECG can rule out cardiac disease in the ED. The initial ECG is normal in approximately 20 percent of patients subsequently diagnosed with a myocardial infarction, and only 33 percent of initial ECGs are diagnostic. The ECG may also reveal signs of pulmonary embolism (PE) (right heart strain), pericardial effusion (diffuse low voltage (waveform 2), electrical alternans (waveform 3)), and other disease processes. However, the sensitivity and specificity of the ECG for PE is limited. It is helpful to compare the ECG with prior studies. (See "Diagnosis of acute myocardial infarction" and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Diagnosis an




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Cardiac biomarkers — Elevated biomarkers support the diagnosis of cardiac ischemia. However, the initial cardiac biomarkers (eg, troponin I) obtained in the ED are frequently normal. Serial measurements of cardiac biomarkers are necessary to rule out an acute coronary syndrome (ACS). Cardiac biomarkers have limited specificity and may be elevated in the setting of PE, sepsis, pericarditis, myocarditis, warfarin use, renal failure, and interference with the assay (generally from monoclonal antibodies or rheumatoid factor).
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rdial infarction" and "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism" and "Diagnosis and treatment of pericardial effusion".) <span>Cardiac biomarkers — Elevated biomarkers support the diagnosis of cardiac ischemia. However, the initial cardiac biomarkers (eg, troponin I) obtained in the ED are frequently normal. Serial measurements of cardiac biomarkers are necessary to rule out an acute coronary syndrome (ACS). Cardiac biomarkers have limited specificity and may be elevated in the setting of PE, sepsis, pericarditis, myocarditis, warfarin use, renal failure, and interference with the assay (generally from monoclonal antibodies or rheumatoid factor). (See "Troponin testing: Clinical use" and "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".) Brain natriuretic peptide (BNP) — The measurement of B




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Brain natriuretic peptide (BNP) — The measurement of BNP may be helpful when the diagnosis of ADHF is in question. However, it can be elevated secondary to many causes of fluid overload, such as renal failure. BNP testing is not helpful when used indiscriminately in patients with acute dyspnea [32]. The length of stay of patients presenting to the ED with acute dyspnea may be slightly reduced if BNP testing is performed [33].
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y (generally from monoclonal antibodies or rheumatoid factor). (See "Troponin testing: Clinical use" and "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".) <span>Brain natriuretic peptide (BNP) — The measurement of BNP may be helpful when the diagnosis of ADHF is in question. However, it can be elevated secondary to many causes of fluid overload, such as renal failure. BNP testing is not helpful when used indiscriminately in patients with acute dyspnea [32]. The length of stay of patients presenting to the ED with acute dyspnea may be slightly reduced if BNP testing is performed [33]. A BNP of less than 100 pg/mL has a negative predictive value of over 90 percent for ADHF. Likewise, a BNP above 500 pg/mL strongly suggests ADHF, with a positive predictive value over 9




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A BNP of less than 100 pg/mL has a negative predictive value of over 90 percent for ADHF. Likewise, a BNP above 500 pg/mL strongly suggests ADHF, with a positive predictive value over 90 percent. A level between 100 pg/mL and 500 pg/mL cannot differentiate between ADHF and other causes of elevated BNP. Causes of a false-positive BNP (generally between 100 pg/mL and 500 pg/mL) include PE, fluid overload states (eg, renal failure, liver failure), critical illness, and other causes of right ventricular distension (eg, cor pulmonale, pulmonary hypertension).
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when used indiscriminately in patients with acute dyspnea [32]. The length of stay of patients presenting to the ED with acute dyspnea may be slightly reduced if BNP testing is performed [33]. <span>A BNP of less than 100 pg/mL has a negative predictive value of over 90 percent for ADHF. Likewise, a BNP above 500 pg/mL strongly suggests ADHF, with a positive predictive value over 90 percent. A level between 100 pg/mL and 500 pg/mL cannot differentiate between ADHF and other causes of elevated BNP. Causes of a false-positive BNP (generally between 100 pg/mL and 500 pg/mL) include PE, fluid overload states (eg, renal failure, liver failure), critical illness, and other causes of right ventricular distension (eg, cor pulmonale, pulmonary hypertension). (See "Natriuretic peptide measurement in heart failure".) D-dimer — A d-dimer is not part of the workup of every patient with chest pain or shortness of breath. Clinical judgment must b




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D-dimer — A d-dimer is not part of the workup of every patient with chest pain or shortness of breath. Clinical judgment must be exercised. Use of the d-dimer depends upon the patient's pretest probability for PE. Patients at low risk for PE according to a validated scoring system (eg, modified Wells criteria for PE, PE rule-out criteria [PERC rule]) and a negative enzyme-linked immunosorbent assay (ELISA) d-dimer can be ruled out for PE without further testing. It is not appropriate to use a d-dimer to screen patients at moderate or high risk for thromboembolic disease. Patients with malignancy or recent surgery and older adult patients are more likely to have a falsely elevated d-dimer.
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ailure, liver failure), critical illness, and other causes of right ventricular distension (eg, cor pulmonale, pulmonary hypertension). (See "Natriuretic peptide measurement in heart failure".) <span>D-dimer — A d-dimer is not part of the workup of every patient with chest pain or shortness of breath. Clinical judgment must be exercised. Use of the d-dimer depends upon the patient's pretest probability for PE. Patients at low risk for PE according to a validated scoring system (eg, modified Wells criteria for PE, PE rule-out criteria [PERC rule]) and a negative enzyme-linked immunosorbent assay (ELISA) d-dimer can be ruled out for PE without further testing. It is not appropriate to use a d-dimer to screen patients at moderate or high risk for thromboembolic disease. Patients with malignancy or recent surgery and older adult patients are more likely to have a falsely elevated d-dimer. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".) Arterial and venous blood gas — The role of the arterial blood




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Arterial and venous blood gas — The role of the arterial blood gas in the diagnosis and treatment of the acutely dyspneic patient is limited. Oxygenation is easily assessed using transcutaneous pulse oximetry. Acid-base status can be assessed using a venous blood gas and the serum bicarbonate. (See "Arterial blood gases" and "Venous blood gases and other alternatives to arterial blood gases".)

A venous blood gas may be useful in the assessment of the patient presumed to be somnolent from CO2 retention. In many patients the presence of CO2 retention can be determined using end-tidal CO2 monitors. The partial pressure of carbon dioxide (PaCO2) should be low in the acutely dyspneic patient, who is usually hyperventilating. A normal or elevated CO2 in the setting of dyspnea and tachypnea portends respiratory failure

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der adult patients are more likely to have a falsely elevated d-dimer. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism".) <span>Arterial and venous blood gas — The role of the arterial blood gas in the diagnosis and treatment of the acutely dyspneic patient is limited. Oxygenation is easily assessed using transcutaneous pulse oximetry. Acid-base status can be assessed using a venous blood gas and the serum bicarbonate. (See "Arterial blood gases" and "Venous blood gases and other alternatives to arterial blood gases".) A venous blood gas may be useful in the assessment of the patient presumed to be somnolent from CO2 retention. In many patients the presence of CO2 retention can be determined using end-tidal CO2 monitors. The partial pressure of carbon dioxide (PaCO2) should be low in the acutely dyspneic patient, who is usually hyperventilating. A normal or elevated CO2 in the setting of dyspnea and tachypnea portends respiratory failure. Carbon dioxide monitoring — Capnography (ie, end-tidal CO2) provides dynamic monitoring of ventilatory status in patients with acute respiratory distress. By measuring end-tidal CO2 (E




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Carbon dioxide monitoring — Capnography (ie, end-tidal CO2) provides dynamic monitoring of ventilatory status in patients with acute respiratory distress. By measuring end-tidal CO2 (EtCO2) and respiratory rate with each breath, capnography provides instantaneous feedback on the clinical status of the patient, while trends enable the clinician to determine whether the patient's ventilation is worsening despite treatment (increasing EtCO2), stabilizing (stable EtCO2), or improving (decreasing EtCO2).
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on dioxide (PaCO2) should be low in the acutely dyspneic patient, who is usually hyperventilating. A normal or elevated CO2 in the setting of dyspnea and tachypnea portends respiratory failure. <span>Carbon dioxide monitoring — Capnography (ie, end-tidal CO2) provides dynamic monitoring of ventilatory status in patients with acute respiratory distress. By measuring end-tidal CO2 (EtCO2) and respiratory rate with each breath, capnography provides instantaneous feedback on the clinical status of the patient, while trends enable the clinician to determine whether the patient's ventilation is worsening despite treatment (increasing EtCO2), stabilizing (stable EtCO2), or improving (decreasing EtCO2). (See "Carbon dioxide monitoring (capnography)".) Chest CT and V/Q scan — A multidetector computed tomography (MDCT) scan of the chest can be used to diagnose multiple problems, includin




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Chest CT and V/Q scan — A multidetector computed tomography (MDCT) scan of the chest can be used to diagnose multiple problems, including PE, malignancy, pneumonia, and pulmonary edema. Often these diseases can be diagnosed by history, examination, and basic testing, without the use of MDCT. MDCT entails some risk, including contrast-induced nephropathy, allergic reaction to contrast, and radiation-related malignancy, and should be used with discretion. However, contrast-related kidney injury is relatively uncommon, and MDCT should be performed, even in patients with compromised renal function, when the study is needed to establish an important diagnosis. Ventilation-perfusion (V/Q) scanning is an alternative method for diagnosing PE in patients unsuitable for MDCT who have a normal chest radiograph and are clinically stable.
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hether the patient's ventilation is worsening despite treatment (increasing EtCO2), stabilizing (stable EtCO2), or improving (decreasing EtCO2). (See "Carbon dioxide monitoring (capnography)".) <span>Chest CT and V/Q scan — A multidetector computed tomography (MDCT) scan of the chest can be used to diagnose multiple problems, including PE, malignancy, pneumonia, and pulmonary edema. Often these diseases can be diagnosed by history, examination, and basic testing, without the use of MDCT. MDCT entails some risk, including contrast-induced nephropathy, allergic reaction to contrast, and radiation-related malignancy, and should be used with discretion. However, contrast-related kidney injury is relatively uncommon, and MDCT should be performed, even in patients with compromised renal function, when the study is needed to establish an important diagnosis. Ventilation-perfusion (V/Q) scanning is an alternative method for diagnosing PE in patients unsuitable for MDCT who have a normal chest radiograph and are clinically stable. (See "Prevention of contrast-induced acute kidney injury associated with computed tomography".) Peak flow and pulmonary function tests (PFTs) — The peak expiratory flow rate (PEFR) can




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Peak flow and pulmonary function tests (PFTs) — The peak expiratory flow rate (PEFR) can be helpful in distinguishing pulmonary and cardiac causes of dyspnea and determining the severity of bronchoconstriction in cases of severe asthma. Keep in mind that normal values vary with gender, height, and age (table 4 and table 5 and table 6), and accuracy depends upon patient cooperation.

Small observational studies suggest PEFR is generally higher in patients with a cardiac cause of dyspnea [34,35]. During acute asthma exacerbations, PEFR measurements provide a screening tool for the presence of hypercapnia and obviate the need for routine blood gases. In the absence of respiratory depressant medications (eg, narcotics or sedatives), hypercapnia is rarely present until the PEFR falls below 25 percent of normal or 200 L/minute. Bedside spirometry is less prone to error but may be difficult to perform in the ED.

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PE in patients unsuitable for MDCT who have a normal chest radiograph and are clinically stable. (See "Prevention of contrast-induced acute kidney injury associated with computed tomography".) <span>Peak flow and pulmonary function tests (PFTs) — The peak expiratory flow rate (PEFR) can be helpful in distinguishing pulmonary and cardiac causes of dyspnea and determining the severity of bronchoconstriction in cases of severe asthma. Keep in mind that normal values vary with gender, height, and age (table 4 and table 5 and table 6), and accuracy depends upon patient cooperation. Small observational studies suggest PEFR is generally higher in patients with a cardiac cause of dyspnea [34,35]. During acute asthma exacerbations, PEFR measurements provide a screening tool for the presence of hypercapnia and obviate the need for routine blood gases. In the absence of respiratory depressant medications (eg, narcotics or sedatives), hypercapnia is rarely present until the PEFR falls below 25 percent of normal or 200 L/minute. Bedside spirometry is less prone to error but may be difficult to perform in the ED. (See "Peak expiratory flow monitoring in asthma".) Negative inspiratory force (NIF) — NIF and forced vital capacity measurements can be obtained at the bedside to assess dyspneic patien




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Negative inspiratory force (NIF) — NIF and forced vital capacity measurements can be obtained at the bedside to assess dyspneic patients with possible neuromuscular disease (eg, myasthenia gravis, Guillain-Barré) or musculoskeletal disease (ankylosing spondylitis, severe scoliosis, or kyphosis). If the NIF is less than 30 cm H2O or the forced vital capacity is less than 15 to 20 mL/kg, the patient should be admitted to an intensive care unit in anticipation of the need for mechanical ventilation [36]. These numbers are guidelines only and do not always predict which patients need respiratory support.
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he PEFR falls below 25 percent of normal or 200 L/minute. Bedside spirometry is less prone to error but may be difficult to perform in the ED. (See "Peak expiratory flow monitoring in asthma".) <span>Negative inspiratory force (NIF) — NIF and forced vital capacity measurements can be obtained at the bedside to assess dyspneic patients with possible neuromuscular disease (eg, myasthenia gravis, Guillain-Barré) or musculoskeletal disease (ankylosing spondylitis, severe scoliosis, or kyphosis). If the NIF is less than 30 cm H2O or the forced vital capacity is less than 15 to 20 mL/kg, the patient should be admitted to an intensive care unit in anticipation of the need for mechanical ventilation [36]. These numbers are guidelines only and do not always predict which patients need respiratory support. (See "Tests of respiratory muscle strength".) MANAGEMENT Initial interventions and differential diagnosis — For any patient with acute severe dyspnea, the following measures are perform




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Initial interventions and differential diagnosis — For any patient with acute severe dyspnea, the following measures are performed immediately:

Oxygen is provided.

Intravenous (IV) access is established and blood obtained for laboratory measurements.

Cardiac and pulse oximetry monitoring is instituted.

Airway management equipment is brought to the bedside.

Screening examination is performed, including an assessment of airway difficulty and a search for rapidly reversible causes (tension pneumothorax, pericardial tamponade, upper airway foreign body).

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ed for mechanical ventilation [36]. These numbers are guidelines only and do not always predict which patients need respiratory support. (See "Tests of respiratory muscle strength".) MANAGEMENT <span>Initial interventions and differential diagnosis — For any patient with acute severe dyspnea, the following measures are performed immediately: ●Oxygen is provided. ●Intravenous (IV) access is established and blood obtained for laboratory measurements. ●Cardiac and pulse oximetry monitoring is instituted. ●Airway management equipment is brought to the bedside. ●Screening examination is performed, including an assessment of airway difficulty and a search for rapidly reversible causes (tension pneumothorax, pericardial tamponade, upper airway foreign body). (See "Approach to the anatomically difficult airway in adults outside the operating room".) Bedside ultrasound is an excellent tool for rapidly determining the presence of pericardial t




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Common life-threatening causes of dyspnea to be considered in all cases include:

● Acute coronary syndrome

● Acute heart failure

● Arrhythmia

● Pericardial tamponade

● Pulmonary embolism (PE)

● Pneumonia or other infection

● Chronic obstructive pulmonary disease (COPD) exacerbation

● Asthma

● Angioedema and anaphylaxis

● Poisoning (eg, carbon monoxide)

● Trauma (eg, pneumothorax, hemothorax)

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ement related to COVID-19 are discussed in a number of UpToDate topics. (See "COVID-19: Clinical features" and "COVID-19: Diagnosis" and "COVID-19: Critical care and airway management issues".) <span>Common life-threatening causes of dyspnea to be considered in all cases include: ●Acute coronary syndrome ●Acute heart failure ●Arrhythmia ●Pericardial tamponade ●Pulmonary embolism (PE) ●Pneumonia or other infection ●Chronic obstructive pulmonary disease (COPD) exacerbation ●Asthma ●Angioedema and anaphylaxis ●Poisoning (eg, carbon monoxide) ●Trauma (eg, pneumothorax, hemothorax) A more complete list of potential diagnoses is provided above. (See 'Differential diagnosis' above.) Emergency management — Three primary goals exist for the emergency clinician faced w




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Emergency management — Three primary goals exist for the emergency clinician faced with an acutely dyspneic patient:

● Optimize arterial oxygenation

● Determine the need for emergency airway management and ventilatory support

● Establish the most likely causes of dyspnea and initiate treatment

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dema and anaphylaxis ●Poisoning (eg, carbon monoxide) ●Trauma (eg, pneumothorax, hemothorax) A more complete list of potential diagnoses is provided above. (See 'Differential diagnosis' above.) <span>Emergency management — Three primary goals exist for the emergency clinician faced with an acutely dyspneic patient: ●Optimize arterial oxygenation ●Determine the need for emergency airway management and ventilatory support ●Establish the most likely causes of dyspnea and initiate treatment The initial decision to provide noninvasive or invasive ventilatory support is made based upon clinical grounds, not laboratory values. Emergency airway management is discussed in detai




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The initial decision to provide noninvasive or invasive ventilatory support is made based upon clinical grounds, not laboratory values. Emergency airway management is discussed in detail elsewhere.
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dyspneic patient: ●Optimize arterial oxygenation ●Determine the need for emergency airway management and ventilatory support ●Establish the most likely causes of dyspnea and initiate treatment <span>The initial decision to provide noninvasive or invasive ventilatory support is made based upon clinical grounds, not laboratory values. Emergency airway management is discussed in detail elsewhere. (See "The decision to intubate" and "Rapid sequence intubation for adults outside the operating room" and "Approach to the anatomically difficult airway in adults outside the operating




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Oxygen is a potent and readily available treatment for many causes of dyspnea and should be administered as clinically indicated. For patients with mild dyspnea and normal room-air arterial oxygen saturation (SpO2), 2 liters per minute (LPM) of oxygen via nasal cannula is typically adequate. For hypoxic patients with respiratory difficulty, 50 to 60 LPM of oxygen should be provided via a nonrebreather mask. To deliver this much oxygen, open the flow meter valve until the indicator lies well beyond the 15 LPM mark. An SpO2 of 94 percent is an appropriate target for most patients.
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e intubation for adults outside the operating room" and "Approach to the anatomically difficult airway in adults outside the operating room" and "Emergency cricothyrotomy (cricothyroidotomy)".) <span>Oxygen is a potent and readily available treatment for many causes of dyspnea and should be administered as clinically indicated. For patients with mild dyspnea and normal room-air arterial oxygen saturation (SpO2), 2 liters per minute (LPM) of oxygen via nasal cannula is typically adequate. For hypoxic patients with respiratory difficulty, 50 to 60 LPM of oxygen should be provided via a nonrebreather mask. To deliver this much oxygen, open the flow meter valve until the indicator lies well beyond the 15 LPM mark. An SpO2 of 94 percent is an appropriate target for most patients. Patients breathing 100 percent oxygen deliver five times as much oxygen to the alveoli per unit of ventilation as those breathing room air and in the absence of parenchymal disease can




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Patients breathing 100 percent oxygen deliver five times as much oxygen to the alveoli per unit of ventilation as those breathing room air and in the absence of parenchymal disease can maintain a normal SpO2 with only two or three breaths per minute. Note, however, that the best nonrebreather oxygen-delivery systems provide only 85 percent oxygen.
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onrebreather mask. To deliver this much oxygen, open the flow meter valve until the indicator lies well beyond the 15 LPM mark. An SpO2 of 94 percent is an appropriate target for most patients. <span>Patients breathing 100 percent oxygen deliver five times as much oxygen to the alveoli per unit of ventilation as those breathing room air and in the absence of parenchymal disease can maintain a normal SpO2 with only two or three breaths per minute. Note, however, that the best nonrebreather oxygen-delivery systems provide only 85 percent oxygen. Do not withhold oxygen from patients with COPD. The target oxygen saturation in such patients is 90 to 94 percent with the understanding that this may reduce ventilatory drive and cause




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Do not withhold oxygen from patients with COPD. The target oxygen saturation in such patients is 90 to 94 percent with the understanding that this may reduce ventilatory drive and cause hypercarbia. However, failure to oxygenate the patient may have profoundly adverse consequences. If a clinician determines that a COPD patient requires endotracheal intubation, oxygen delivery should be maximized without regard for the target oxygen saturation or hypercarbia.
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e of parenchymal disease can maintain a normal SpO2 with only two or three breaths per minute. Note, however, that the best nonrebreather oxygen-delivery systems provide only 85 percent oxygen. <span>Do not withhold oxygen from patients with COPD. The target oxygen saturation in such patients is 90 to 94 percent with the understanding that this may reduce ventilatory drive and cause hypercarbia. However, failure to oxygenate the patient may have profoundly adverse consequences. If a clinician determines that a COPD patient requires endotracheal intubation, oxygen delivery should be maximized without regard for the target oxygen saturation or hypercarbia. Note that excessive oxygen may be harmful in those with acute coronary syndrome (ACS). Administer oxygen for ACS only when the oxygen saturation is consistently below 94 percent. (See "




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Note that excessive oxygen may be harmful in those with acute coronary syndrome (ACS). Administer oxygen for ACS only when the oxygen saturation is consistently below 94 percent.
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consequences. If a clinician determines that a COPD patient requires endotracheal intubation, oxygen delivery should be maximized without regard for the target oxygen saturation or hypercarbia. <span>Note that excessive oxygen may be harmful in those with acute coronary syndrome (ACS). Administer oxygen for ACS only when the oxygen saturation is consistently below 94 percent. (See "COPD exacerbations: Management" and "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure" and "Overview of the acute managemen




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Noninvasive ventilation does not improve outcomes in patients with acute exacerbations of asthma and diseases that do not respond rapidly to medical therapy (eg, pneumonia and acute respiratory distress syndrome [ARDS]). In such instances, endotracheal intubation and controlled mechanical ventilation should be pursued aggressively when ventilatory support is needed.
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cerbation. (See "Noninvasive ventilation in adults with acute respiratory failure: Benefits and contraindications" and "Treatment of acute decompensated heart failure: General considerations".) <span>Noninvasive ventilation does not improve outcomes in patients with acute exacerbations of asthma and diseases that do not respond rapidly to medical therapy (eg, pneumonia and acute respiratory distress syndrome [ARDS]). In such instances, endotracheal intubation and controlled mechanical ventilation should be pursued aggressively when ventilatory support is needed. (See "Acute exacerbations of asthma in adults: Home and office management" and "Treatment of community-acquired pneumonia in adults who require hospitalization" and "Acute respiratory d




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As examples, an improvement in SpO2 immediately after the administration of low-flow oxygen indicates a ventilation-perfusion (V/Q) mismatch, while rapid improvement following treatment with bronchodilators strongly suggests bronchoconstriction. Failure to improve with oxygen administration may indicate a right to left shunt.
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ent".) As with all life-threatening complaints, dyspnea is managed by clinicians performing therapeutic interventions and diagnostic assessment concurrently. Often therapy assists in diagnosis. <span>As examples, an improvement in SpO2 immediately after the administration of low-flow oxygen indicates a ventilation-perfusion (V/Q) mismatch, while rapid improvement following treatment with bronchodilators strongly suggests bronchoconstriction. Failure to improve with oxygen administration may indicate a right to left shunt. (See "Measures of oxygenation and mechanisms of hypoxemia".) An electrocardiogram (ECG) and stat portable chest radiograph (CXR) should be obtained early in the course of management whe




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When managing a life-threatening complaint with a broad differential diagnosis such as severe, acute dyspnea, it is crucial that emergency clinicians not fall prey to premature diagnostic closure. Clinical, laboratory, and radiographic findings that contradict the clinician's initial impressions must be carefully considered.
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rventions may include broad-spectrum antibiotics when infection is suspected or stress-dose glucocorticoids for patients who use such medications chronically (eg, patients with chronic asthma). <span>When managing a life-threatening complaint with a broad differential diagnosis such as severe, acute dyspnea, it is crucial that emergency clinicians not fall prey to premature diagnostic closure. Clinical, laboratory, and radiographic findings that contradict the clinician's initial impressions must be carefully considered. Nonemergency management — In most instances, the emergency clinician can determine the diagnosis or the need for hospital admission based upon a thorough history, physical examination,




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Often the cause of dyspnea cannot be determined with certainty in the ED. In such cases, the clinician's job is to treat and appropriately triage the patient based upon the clinical scenario and an assessment of the patient's risk. High-risk dyspneic patients include older adults and those who are immunocompromised, have severe underlying lung or heart disease, or demonstrate unexplained abnormal vital signs.
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ascular system. Common, potentially life-threatening causes of dyspnea should be considered in all cases. These are listed above. (See 'Initial interventions and differential diagnosis' above.) <span>Often the cause of dyspnea cannot be determined with certainty in the ED. In such cases, the clinician's job is to treat and appropriately triage the patient based upon the clinical scenario and an assessment of the patient's risk. High-risk dyspneic patients include older adults and those who are immunocompromised, have severe underlying lung or heart disease, or demonstrate unexplained abnormal vital signs. DISPOSITION — The patient's condition, preliminary diagnosis, and risk assessment determine disposition. Patients with severe disease or those at risk of rapid deterioration who require




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The patient's condition, preliminary diagnosis, and risk assessment determine disposition. Patients with severe disease or those at risk of rapid deterioration who require close monitoring should be admitted to an intensive care setting. Those with less severe disease but who fail to improve with treatment in the emergency department (ED) or who have significant comorbidities or risk factors are admitted to the appropriate hospital ward.

Stable patients whose evaluation has ruled out significant disease or determined that the risk for such disease is acceptably low may be discharged. Patients being discharged must have a clear understanding of their discharge diagnosis, written discharge instructions, and planned follow-up with clear instructions to return to the ED if their condition worsens. Particularly with older adult patients, the clinician must consider such factors as the patient's living situation and access to medical follow-up when determining the appropriateness of discharge.

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igh-risk dyspneic patients include older adults and those who are immunocompromised, have severe underlying lung or heart disease, or demonstrate unexplained abnormal vital signs. DISPOSITION — <span>The patient's condition, preliminary diagnosis, and risk assessment determine disposition. Patients with severe disease or those at risk of rapid deterioration who require close monitoring should be admitted to an intensive care setting. Those with less severe disease but who fail to improve with treatment in the emergency department (ED) or who have significant comorbidities or risk factors are admitted to the appropriate hospital ward. Stable patients whose evaluation has ruled out significant disease or determined that the risk for such disease is acceptably low may be discharged. Patients being discharged must have a clear understanding of their discharge diagnosis, written discharge instructions, and planned follow-up with clear instructions to return to the ED if their condition worsens. Particularly with older adult patients, the clinician must consider such factors as the patient's living situation and access to medical follow-up when determining the appropriateness of discharge. PITFALLS IN MANAGEMENT ●Failure to secure the airway in a timely manner ●Failure to recognize and act on abnormal vital signs and signs of impending respiratory failure ●Over-reliance u




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● 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, COPD, PE, and asthma.
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eumonia or other infection •Chronic obstructive pulmonary disease (COPD) exacerbation •Asthma •Angioedema and anaphylaxis •Poisoning (eg, carbon monoxide) •Trauma (eg, pneumothorax, hemothorax) <span>●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, COPD, PE, and asthma. (See 'Epidemiology' above.) ●Important elements of the history and physical examination in patients with acute dyspnea are described in the text. (See 'History' above and 'Physical exam