AACN Advanced Critical Care Volume 25, Number 3, pp. 284-290 © 2014 AACN

The Challenge of Diagnosing Dyspnea Beth Croucher, RN, MS, ACNP-BC

ABSTRACT Dyspnea is a subjective and nonspecific symptom, yet very distressing for those who experience it. Acute onset dyspnea and exacerbation of chronic dyspnea from heart or lung disease significantly add to the number of emergency department visits and inpatient admissions. Although dyspnea may appear to be a simple condition to evaluate and manage, it is actually complex in description and quality. As such, dyspnea is the first symptom of many diseases. The

onset of dyspnea can be due to a new acute disease, the exacerbation of an existing chronic illness, or a new disease compounding a chronic illness. Finding the cause of dyspnea is generally more difficult than it originally may appear. Therefore, the purpose of this article is to discuss the differential diagnoses associated with dyspnea. Keywords: differential diagnosis, dyspnea, respiratory distress, respiratory exacerbation, shortness of breath

commonly used term that is interchangeable with dyspnea. The most widely recognized definition of dyspnea is from the American Thoracic Society, which describes dyspnea as “a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.”1(p436) Dyspnea is a common problem in chronic cardiac and lung disease, in certain acute disease states, and among obese and elderly populations during activities of daily living. The presence of dyspnea is a predictor of hospitalization.2 The most prevalent symptom reported by patients with chronic obstructive pulmonary disease (COPD) is dyspnea. Almost 70% of patients with COPD questioned in a telephone survey reported shortness of breath when walking up 1 flight of stairs.3 Patients are reliable in reporting levels of dyspnea that correspond with severity of chronic diseases such as COPD.4

Case Study: A 56-year-old woman presented to the emergency department with a chief complaint of “not getting enough air.” She stated that she had had this feeling “for a few days”; however, the feeling had gotten progressively worse, causing her to seek treatment in the emergency department. Additional symptoms included increased cough without sputum production along with increasing fatigue and loss of appetite. She denied chest pain or fever. She admitted to a smoking history of 1 pack per day for 40 years. When questioned about her medical history, she stated that she might have been told she had high blood pressure, but she could not remember. She did not have a primary care provider and did not seek regular health care. Physical examination revealed a heart rate of 124 beats/min and a respiratory rate of 28 breaths/ min. Her pulse oximetry read 85% on room air. Her lung sounds were clear but diminished bilaterally in the lung bases. Heart sounds were regular with no murmur.

Definition and Occurrence of Dyspnea The presenting symptom of this patient is her subjective feeling of “not getting enough air,” and that is one description of the symptom of dyspnea. The term shortness of breath is a

Beth Croucher is Nurse Practitioner, Medical Intensive Care, Department of Pulmonary/Critical Care, Ohio State University Wexner Medical Center, 410 W 10th Ave, Columbus, OH 43210 ([email protected]). The author declares no conflicts of interest. DOI: 10.1097/NCI.0000000000000044

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Mechanism of Dyspnea The mechanism of dyspnea is complex and multifactorial, including physiological, psychological, social, and environmental elements. Dyspnea is not a single sensation but a combination of multiple sensory receptors and neural pathways that are not fully understood.1,5 The respiratory control center of the brain is located in the medulla oblongata and exerts central control over breathing patterns. Peripheral chemoreceptors located near the carotid bodies and mechanoreceptors located in the diaphragm and skeletal muscles detect changes in PaO2, PaCO2, and possibly other by-products of metabolism. A change in the homeostasis of these mechanisms is perceived as the sensation of dyspnea.1 An imbalance between motor signals sent to the respiratory muscles and incoming sensory information likely due to ventilation demands exceeding the ability of the respiratory system to comply produces dyspnea.5 Language of Dyspnea Dyspnea is compared with pain in that they are both subjective symptoms best described and quantified only by individuals at the time they experience the symptom. Describing dyspnea in general terms such as shortness of breath or labored breathing may inadequately describe this symptom to its fullest extent. Evidence suggests that dyspnea can be described with different qualities, much like chest pain is described using differing sensations.6 Awareness and attention to these distinct qualities will assist in finding the cause and treatment options available to relieve the symptom of dyspnea. Together, the descriptors of work of breathing, chest tightness, and air hunger are considered the language of dyspnea.7 A sense of having to work harder to breathe, sometimes described as increased work of breathing or an increased effort to breathe, is most commonly associated with COPD, asthma, and neuromuscular impairment of respiratory muscles.6 These descriptions are similar in quality to the increased work of breathing during exercise and arise from the same mechanism.8 The feeling of increased work of breathing may relate to muscle contraction and increased respiratory muscle fatigue.5 Chest tightness is a descriptor often noted by patients with acute bronchoconstriction, as in an asthma exacerbation. The feeling of chest tightness precedes other descriptors of dyspnea when bronchoconstriction is provoked during

pulmonary function testing.9 Air hunger, the feeling of needing more air, which is also called unsatisfied inspiration, and an uncomfortable urge to breathe are descriptions of dyspnea often used by patients with COPD, restrictive diseases such as pulmonary fibrosis, or exacerbations of heart failure. This feeling is caused by increased ventilatory demand that exceeds available minute ventilation. Often described as distressing or suffocating, air hunger may be induced or exacerbated by anxiety.8 Acute Onset Versus Acute Exacerbation Acute Onset

The presence of dyspnea may be acute in onset, caused by an acute exacerbation of chronic dyspnea, or may be chronic in nature as a result of diseases such as COPD or heart failure (Table 1). When a patient presents with dyspnea, the first step is to determine whether chronic dyspnea is present or whether dyspneic events have previously occurred. In patients who are naive to the sensation of shortness of breath, an episode of acute dyspnea could potentially be life threatening. The rapidity with which the onset of dyspnea is noted is also an indicator of the severity of the pathological condition. When the onset of dyspnea occurs within minutes, differential diagnoses should include myocardial infarction, pulmonary embolism (PE), acute mitral insufficiency, pneumothorax, anaphylaxis, foreign body aspiration, pulmonary edema, or cardiac tamponade.10 Although chest pain and diaphoresis are more commonly associated with acute coronary syndrome, dyspnea occurs in about onethird to one-half of these patients and may be the sole presenting symptom, especially in women.11 Dyspnea in the setting of PE may be accompanied by hypoxemia, pleuritic chest pain, tachycardia, wheezing, friction rub, or lower extremity edema. Symptom presentation will depend on the size and location of the PE. Hypotension also may be present. In patients with COPD and chronic dyspnea, PE was noted in one-fifth of patients with an acute exacerbation of dyspnea.11 The shortness of breath caused by a pneumothorax may be seen with pleuritic chest pain and absence of breath sounds, with hyperresonance to percussion on the affected side.12 Tachypnea is usually present, and hypotension also may occur.11 Acute pulmonary edema may have signs of

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Table 1: Differential Diagnoses of Dyspnea Diagnosis Anaphylaxis

Signs Cough

Symptoms Tightness in upper airways

Stridor Wheezing Obstruction

Cough

Dysphagia

Wheezing Stridor Cyanosis Impaired speech Epiglottitis

Fever

Sore throat

Stridor

Dysphagia

Drooling Tripod positioning (late) Pulmonary embolism

Pulmonary edema

Tachycardia Hypoxemia Tachypnea Hypotension Lower extremity edema Friction rub Frothy sputum, possibly blood tinged

Pleuritic chest pain

Positive hepatojugular reflex

Orthopnea

Chest pain

S3 or S4 heart sounds Pneumothorax

Decreased breath sounds on affected side

Pleuritic chest pain

Hyperresonance on affected side Tachypnea Tachycardia Hypotension Chronic obstructive pulmonary disease

Wheezing

Orthopnea

Cough

Exercise intolerance

Increased sputum production Pursed lip breathing Asthma

Cough

Chest tightness

Wheezing Accessory muscle use with respiration Acute coronary syndrome Acute mitral insufficiency Cardiac tamponade

Diaphoresis

Crushing chest pain

Hypotension

Indigestion

Tachycardia

Nausea

Murmur (not always present)

Fatigue Chest discomfort

Distant heart tones

Chest discomfort

Hypotension Tachycardia Heart failure

Pulmonary crackles

Weight gain

Lower extremity edema

Orthopnea Paroxysmal nocturnal dyspnea

Metabolic acidosis

Neuromuscular disease

Altered mental status

Confusion

Hyperglycemia

Thirst

Electrolyte abnormalities

Fatigue

Progressive symmetrical extremity weakness

Progressive dysphagia

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pink frothy sputum, edema, positive hepatojugular reflex, or S3 or S4 heart sounds.12 Dyspnea associated with cardiac tamponade may have a slower onset depending on the rate at which the pericardium fills with fluid.10 Distant heart sounds, distended neck veins, or hypotension may be present. If acute worsening of shortness of breath occurs in patients with chronic dyspnea at rest, the presence of a new pathological condition must be considered as a cause before attributing the worsening dyspnea to an exacerbation of a chronic condition. The onset of dyspnea over the course of hours to days may be the result of an acute condition or the exacerbation of a chronic condition. Acute conditions that may present as worsening dyspnea over hours to days are pneumonia, epiglottitis, or metabolic acidosis. Patients with pneumonia may have fever and cough with or without sputum production and may exhibit a consolidation on chest radiograph. Epiglottitis may include stridor and drooling along with dyspnea. Fever also may be present. As the edema of epiglottitis worsens, patients may assume a tripod position to assist in ventilation. Tripod positioning can be seen in dyspneic patients because it is a position that optimizes ventilation. Patients will sit up and lean forward while resting their hands on their knees or other surface.13 Dyspnea may be associated with metabolic acidosis from renal failure or diabetic ketoacidosis. In this case, the sensation of breathlessness is caused by hyperventilation caused by the physiological drive of the body to compensate for the metabolic acidosis. If the drive to hyperventilate exceeds the capacity of the respiratory system, then air hunger will be present.12 Altered mentation occurs as acidosis progresses. Urine or serum ketones may be present, and electrolyte abnormalities will be evident, which increases confusion and lethargy. In addition, dyspnea may have a psychogenic cause, as chest tightness and shortness of breath may be caused by a panic or anxiety attack. Patients with chronic dyspnea from COPD may have a rapid onset of dyspnea precipitated by anxiety.14 Acute Exacerbation

Acute exacerbation of chronic disease in patients with COPD or heart failure also may present as worsening breathlessness over the course of hours to days. An exacerbation of heart failure, asthma, or COPD will worsen

chronic dyspnea to a level not usually experienced by patients and will likely motivate them to seek medical treatment.8 The presence of paroxysmal nocturnal dyspnea, which is sudden worsening of dyspnea when lying down, may be a sign of exacerbation of heart failure.15 Patients with paroxysmal nocturnal dyspnea generally wake with acute shortness of breath 1 to 2 hours after going to sleep, and the dyspnea can be somewhat relieved by sitting upright. Worsening orthopnea, which is dyspnea when in a reclined or recumbent position, may signal an exacerbation of COPD or heart failure. Assessing a change in the number of pillows used at night or moving from sleeping in a bed to a chair is useful in determining whether worsening orthopnea is present. In patients with heart failure or COPD, once new acute causes of dyspnea have been ruled out, then an exacerbation of the chronic condition can be considered as the cause of worsening dyspnea. Patients with an exacerbation of heart failure usually have signs of volume overload, including lower extremity edema, weight gain, pulmonary crackles, jugular venous distention, and possibly an S3 gallop. Indications of a COPD exacerbation include wheezing on auscultation, increased cough, and change in color or amount of sputum production. Pursed lip breathing is usually noted, and cyanosis may be present if hypoxemia occurs. Asthma exacerbation also presents with wheezing and cough and is accompanied by chest tightness and accessory muscle use and tachypnea.11 Progression of Chronic Disease

Chronic diseases such as COPD, heart failure, cardiomyopathy, pulmonary fibrosis, pulmonary hypertension, chronic anemia, and neuromuscular diseases such as amyotrophic lateral sclerosis are generally associated with varying levels of chronic dyspnea. Although exacerbations of dyspnea associated with these diseases may occur, patients also can experience increasing levels of dyspnea as disease progression occurs. As the disease worsens, differentiating the cause of dyspnea between an acute exacerbation and progression of disease becomes increasingly difficult. The goal for this patient population is outpatient management with reevaluation of severity of disease at periodic intervals, with adjustments in the treatment regimen. Patients may have multiple comorbid conditions that complicate diagnosing the cause of acute exacerbations that may occur.15

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Assessment of Dyspnea Direct assessment of dyspnea includes prioritizing several different steps. Hemodynamic stability is the initial priority assessment, followed by a thorough medical history and appropriate diagnostic testing. Hemodynamic Stability

The initial assessment for a patient with acute dyspnea focuses on hemodynamic stability. Rapid evaluation for impending respiratory failure is essential. Signs of impending respiratory failure include strained fragmented speech, tripod positioning, diaphoresis, and cyanosis. Hypoxemia, especially with a PaO2 less than 50 mm Hg, may be evident by signs of altered cognition.16 Hypoventilation, particularly if the PaCO2 rises above 70 mm Hg,17 also will cause altered or depressed mental status. Hyperventilation with increased work of breathing and use of accessory muscles may be noted, or retractions consisting of depression of skin over the chest wall during inspiration may be apparent. The appearance of any of these signs indicates that respiratory failure is occurring and immediate intervention is required, which may include noninvasive positive pressure ventilation or intubation. Hypotension, in combination with dyspnea, indicates the threat of cardiopulmonary collapse and the need for resuscitation. Medical History

If the patient is hemodynamically stable and without signs of significant distress, further evaluation for the cause of the dyspnea crisis is warranted. Because dyspnea is a nonspecific symptom, a thorough history is pivotal in directing further workup and ascertaining the cause. Obtaining a history may be difficult in the midst of acute dyspnea, because the patient may have difficulty speaking in full sentences; therefore, the assistance of family members or a review of medical records may be needed. Medical history of COPD, heart failure, coronary artery disease, smoking history, or exposure to secondhand smoke or environmental chemical exposures even in the absence of prior episodes of dyspnea will assist in guiding a diagnostic workup. Determine whether the patient has ever experienced a similar episode and what events transpired around that event, including if a previous intubation was required. Ask whether this event is similar to previous events. Questions about this specific episode

also are critical. Was there an antecedent to this event? Were there any changes in diet, medications, smoking patterns, or any unusual events preceding the occurrence of dyspnea? Another important factor is whether this episode of dyspnea developed over a period of hours or days. Sudden onset dyspnea will lead the diagnostic course to rule out acute causes such as PE, whereas dyspnea that worsens over several days is more likely an exacerbation of a chronic condition. Question possible changes in weight, level of activity, fatigue, or breathlessness in the days before seeking medical attention. Include questions in the subjective assessment about chest pain, sore throat, cough with or without sputum production, fever, orthopnea, and indigestion.12 Laboratory Diagnostics

Information obtained from the history and physical assessment will determine the most applicable diagnostic studies. Various blood tests may be useful in locating 1 or more of the causes of dyspnea. In an unstable patient at risk of respiratory failure, an arterial blood gas test will evaluate the level of hypoxemia or hypercarbia. A complete blood cell count will assess anemia as a causative factor as well as leukocytosis as an indicator of infection. Measure troponin isoforms if acute coronary syndrome is a concern. The D-dimer test should be included in the laboratory workup if PE is suspected.18 D-dimer is a product of fibrin degradation in the breakdown of blood clots and can be measured in venous blood.11 Use of the D-dimer assay varies because of its lack of specificity, and the negative predictive value of this test is most useful in an outpatient setting when used in conjunction with a clinical assessment for the probability of PE, such as the Wells criteria. The Wells criteria are guidelines for determining the probability of PE when clinical presentation of a patient includes PE in the differential diagnoses. Points are assigned for particular characteristics or symptoms, including active cancer diagnosis, surgery, or event causing the patient to be bedbound for more than 3 days over the 4 weeks prior to presentation; history of PE or deep vein thrombosis; heart rate greater than 100 beats/min; signs and symptoms of deep vein thrombosis, including pain, edema, or erythema of an extremity; or if PE is considered the most likely diagnosis. Each of these characteristics is scored, and the total score indicates

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whether the probability of PE is low, moderate, or high.19 The utility of the Wells criteria, in conjunction with the D-dimer, is greatest in the setting of a patient with rapid onset acute dyspnea who is seeking initial medical intervention.8,19 The validity of the D-dimer diminishes greatly for patients who are already hospitalized,19,20 especially if it has been more than a few days since the admission, and the patient is older than 60 years.20 Brain-type natriuretic peptide (BNP) is a neurohormone released from cardiac cells in the ventricles in response to volume overload and the pressure of ventricular overexpansion.8,11 N-terminal prohormone precursor is a related peptide that, along with BNP, may indicate heart failure as a cause of dyspnea.8 Although heart failure is the most likely cause of an elevated BNP, other disease states, including obstructive sleep apnea, PE, valvular heart disease, pulmonary artery hypertension, or sepsis, may influence the BNP level.11 Use of BNP incorporated in the evaluation of heart failure as a cause of acute dyspnea may lead to improved treatment and decreased hospital admission.21 Diagnostic Studies

When acute coronary syndrome is suspected as a cause of dyspnea, a 12-lead electrocardiogram is an essential component of diagnosis, along with the troponin isoform level, and should be included if an ischemic cardiac event is suspected, even in the absence of chest pain.11 Radiograph of the chest commonly is used as a diagnostic tool in patients with acute dyspnea. Evidence of parenchymal consolidations, pneumothorax, pleural effusions, or pulmonary edema may be noted on a plain chest film, which is a useful tool in finding the cause of undifferentiated acute dyspnea. Cardiomegaly or elongated lung fields may confirm the presence of chronic heart or lung disease, providing grounds for further workup of previously undiagnosed disease. Echocardiography is a quick, noninvasive method of evaluating the presence and severity of heart failure. Echocardiography results, along with the BNP and clinical presentation, may provide proof of heart failure exacerbation or pulmonary hypertension as the cause of dyspnea. In addition, transthoracic echocardiography may be used to evaluate the effect of COPD on the right and left ventricles.22 Chest ultrasonography is gaining favor in emergency

departments and critical care areas as a rapid, noninvasive method of evaluating lung fields. Ultrasound can quickly assess for pleural effusion or pneumothorax at the bedside. Computed tomography (CT) of the chest is beneficial for evaluating acute dyspnea in limited circumstances. It is most effectively used in diagnosing PE. The sensitivity of CT pulmonary angiography is 57% to 100%, while the specificity is 78% to 100% in accurately diagnosing a PE.11 It is widely used but is not without risk, given the potential renal impact of the intravenous contrast required for the examination. High-resolution chest CT is useful in evaluating the severity of pulmonary fibrosis23 and COPD24 in patients with normal radiographs of the chest who experience chronic dyspnea. Pulmonary function testing measures airflow and lung volumes through the use of volume-time spirometry. It is the criterion standard test for diagnosis and staging of restrictive and obstructive lung disease. Pulmonary function testing is contraindicated in acute illness especially if the patient has instability in respiratory or hemodynamic functions. While an essential part of a complete evaluation for chronic dyspnea, it should not be considered a valuable diagnostic tool in the setting of acute dyspnea.13 Case Study Follow-up In the earlier example, the patient was a 56-year-old woman with dyspnea who presented to the emergency department. Additional symptoms were not specific and her medical history was unclear, given her lack of regular follow-up with a provider, which makes finding the cause of her dyspnea more difficult. Diagnosis of the cause of her dyspnea began with a physical assessment for hemodynamic stability. She was tachycardic, tachypneic, and mildly hypoxemic on room air. However, she did not appear to be in respiratory distress. She was not using accessory muscles or tripod positioning to assist with ventilation. No stridor or wheezing was present on auscultation. Her blood pressure was stable. Her oxygen saturation and respiratory rate improved rapidly with the administration of 2 L of oxygen per nasal cannula. She was hemodynamically stable. The differential diagnoses for the cause of this patient’s dyspnea include acute coronary syndrome, PE, pneumonia, and pulmonary

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edema. Acute coronary syndrome is included in the differential list without the presence of chest pain because dyspnea alone may be the presenting symptom from a myocardial infarction.11 A troponin blood test and electrocardiogram were completed and were negative. Although dyspnea occurred over several hours to days, PE is included in the differential list until it can be ruled out. Using the Wells criteria, PE is considered a low probability diagnosis. A D-dimer test was completed, which was negative. Given these findings, PE can be ruled out, so that further testing was not warranted in this patient. Chest radiograph showed an area of atelectasis in her right lung base. No pulmonary edema was evident. A complete blood cell count was done, revealing a normal white blood cell count and hemoglobin. Given the new onset cough and consolidation on the chest radiograph, the most likely cause of dyspnea in this patient was pneumonia. She was treated with oral azithromycin, nebulized albuterol, and inhaled and oral steroids, resulting in reduction in her symptoms. This patient also had a lengthy history of tobacco abuse, and she may have had COPD that had not yet been diagnosed. Once her acute illness was resolved, she would benefit from pulmonary function testing to determine the presence and severity of COPD. Conclusion Dyspnea is a prevalent symptom among patients who seek medical care. Unfortunately for providers, shortness of breath is a nonspecific symptom with multiple descriptions that is present in a wide variety of disease states. The key to understanding the cause of dyspnea is recognizing associated symptoms and the pathological condition to which the symptoms relate. A timely, thorough, and accurate assessment of the history and clinical condition of a patient with dyspnea is imperative, as some medical conditions may be severe or life threatening. Understanding the differential diagnoses of dyspnea and how to quickly and accurately determine the underlying cause is the key to providing relief for patients with dyspnea. REFERENCES 1. American Thoracic Society. Dyspnea: mechanisms, assessment, and management. A consensus statement. Am J Respir Crit Care Med. 1999;159:321–340. 2. Ong KC, Earnest A, Lu SJ. A multidimensional grading system (BODE index) as predictor of hospitalization for COPD. Chest. 2005;128:3810–3816.

3. Rennard S, Decramer M, Calverly PM, et al. The impact of COPD in North America and Europe in 2000: the subject’s perspective of the Confronting COPD International Survey. Eur Respir J. 2002;20:799–805. 4. Mahler DA, Ward J, Waterman LA, McCusker C, ZuWallack R, Baird J. Patient-reported dyspnea in COPD and association with stage of disease. Chest. 2009;136 (6):1473–1479. 5. Nishino T. Dyspnoea: underlying mechanisms and treatment. Br J Anaesth. 2011;106(4):463–474. 6. Simon PM, Schwartzstein RM, Weiss JW, Fencl V, Teghtsoonian M, Weinberger SE. Distinguishable types of dyspnea in patients with shortness of breath. Am Rev Respir Dis. 1990;142:1009–1014. 7. Mahler DA. Do you speak the language of dyspnea? Chest. 2000;117(4):928–929. 8. Parshall M, Schwartzstein R, Adams L, et al. An official American Thoracic Society statement: update on the mechanisms, assessment, and management of dyspnea. Am J Respir Crit Care Med. 2012;184(4):435–452. 9. Moy ML, Weiss JW, Sparrow D, Israel E, Schwartzstein RM. Quality of dyspnea in bronchoconstriction differs from eternal resistive loads. Am J Respir Crit Care Med. 2000;162:451–455. 10. Delzell J. Common lung conditions: acute dyspnea. Am Fam Phys. 2013;409:17–22. 11. Gifford A, Mahler DA. Dyspnea. In: Spiro S, Selvestri G, Agusti A, eds. Clinical Respiratory Medicine, 4th ed. Philadelphia, PA: Elsevier; 2012:Chap 19. 12. Zoorab RJ, Campbell JS. Acute dyspnea in the office. Am Fam Phys. 2003;68(9):1804–1810. 13. Douce FH. Pulmonary function testing. In: Kacmarek RM, Stoller JK, Heuer AJ, eds. Egan’s Fundamentals of Respiratory Care. St Louis, MO: Elsevier; 2013: Chap 19. 14. Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact and treatment. Psychosom Med. 2003;65:963. 15. Braithwaite S, Perina D. Dyspnea. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine. Philadelphia, PA: Elsevier; 2014:Chap 25. 16. Moosavi SH, Golestanina E, Binks AP, Lansing RW, Brown R, Banzett RB. Hypoxic and hypercapnic drives to breathe generate equivalent levels of air hunger in humans. J Appl Physiol. 2003;94:141–154. 17. Dean JB, Mulkey DK, Garcia AJ, Putnam RW, Henderson RA. Neuronal sensitivity to hyperoxia, hypercapnia and inert gases at hyperbaric pressures. J Appl Physiol. 2003;95:883–909. 18. Van Belle A, Buller HR, Huisman MV, et al. Effectiveness of managing suspected pulmonary embolism using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA. 2006;295: 172–179. 19. Kearon C, Ginsberg JS, Douketis J, et al. An evaluation of D-dimer in the diagnosis of pulmonary embolism. Ann Intern Med. 2006;144:812–821. 20. Brotman DJ, Segal JB, Jani JT, Petty BG, Kickler TS. Limitations of D-dimer testing in unselected inpatients with suspected venous thromboembolism. Am J Med. 2003;114:276–282. 21. Mueller C, Scholar A, Laule-Kilian K, et al. Use of b-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med. 2004;350(7):647–654. 22. Singh D. Cardiovascular alteration in COPD—What hurts the patient the most? Chest. 2014;145(3):396A. 23. Wells AU, Hansell DM, Ruben MB, Cullinan P, Black CM, du Bois RM. The predictive value of appearances on thin-section computed tomography in fibrosing alveolitis. Am Rev Respir Dis. 1993;148:1076–1084. 24. Klein JS, Gamsu G, Webb WR, Golden JA, Müller NL. High-resolution CT diagnosis of emphysema in symptomatic patients with normal chest radiographs and isolated low diffusing capacity. Radiology. 1992;182: 817–821.

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The challenge of diagnosing dyspnea.

Dyspnea is a subjective and nonspecific symptom, yet very distressing for those who experience it. Acute onset dyspnea and exacerbation of chronic dys...
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