Primary Care Medicine (Chapter 40: Evaluation of Chronic Dyspnea) PDF

Chapter 40 EVALUATION DYSPNEA OF CHRONIC Dyspnea is the subjective sensation of difficult or uncomfortable breathing. Patients commonly complain of “shortness of breath” to describe their respiratory difficulty. Acute dyspnea is most often a manifestation of sudden left ventricular dysfunction (see...

Chapter 40 EVALUATION DYSPNEA OF CHRONIC Dyspnea is the subjective sensation of difficult or uncomfortable breathing. Patients commonly complain of “shortness of breath” to describe their respiratory difficulty. Acute dyspnea is most often a manifestation of sudden left ventricular dysfunction (see Chapter 32), bronchospasm (see Chapter 48), pneumonia (see Chapter 52), pulmonary embolization (see Chapter 20), or anxiety (see Chapter 226). The patient often presents in the urgent care or emergency room setting. Patients with chronic dyspnea, even when it is severe, are more likely to come to the office for care. Long-standing dyspnea can be evaluated safely in the outpatient setting. This chapter focuses on the patient with chronic dyspnea. The differentiation between heart and lung disease as the cause of dyspnea can be difficult; moreover, these causes often coexist. The reported prevalence of chronic obstructive pulmonary disease (COPD) among patients with congestive heart failure (CHF) ranges from 20% to 32%, depending on the clinical setting in which the study was conducted. In such instances, diagnosis requires determining which condition is predominant. In evaluating the chronically dyspneic patient, one needs to check for precipitants and reversible components in addition to ascertaining the cause. Also important are assessments of functional status and prognosis, which are often closely correlated. Copyright © 2020. Wolters Kluwer Health. All rights reserved. PATHOPHYSIOLOGY PRESENTATION (1–11) AND CLINICAL The pathophysiology of dyspnea is multifactorial and complex. In most instances, dyspnea results from cardiac or pulmonary decompensation and is provoked by the stimulation of receptors responsive to metabolic changes, pulmonary interstitial stretch, respiratory muscle tension, and central respiratory command. Shortness of breath is experienced when ventilatory demand exceeds the actual or perceived capacity of the lungs to respond. The work of breathing may be increased by altered chest wall mechanics, decreased lung compliance, airway obstruction, increased ventilatory requirements, or exogenous factors such as obesity. Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. Congestive Heart Failure (see also Chapter 32) CHF can cause dyspnea as pulmonary capillary pressure rises and fluid accumulates in the interstitium, leading to a fall in pulmonary compliance and a sense of difficulty breathing. The earliest symptom is often dyspnea on exertion. More severe failure is manifested by orthopnea and finally paroxysmal nocturnal dyspnea. Basilar crackles (rales) and a third heart sound (S3) are important signs of left-sided heart failure and pulmonary venous hypertension; the S3 is one of the most specific signs of CHF; a documented S3 has been reported to have a positive likelihood ratio (LR+) for heart failure of 24 (see Chapter 2). Peripheral edema and jugular venous distention are common manifestations of right-sided heart failure, but these findings, particularly leg edema, are very nonspecific (see Chapter 22). Jugular venous distention has LR+ of 8.5. Contributing and precipitating factors include fever, acute ischemia, excessive dietary sodium intake, dysrhythmias, concurrent use of agents that are negatively inotropic (e.g., beta-blockers, disopyramide, verapamil), and poor compliance with medical regimen (see Chapter 32). Community studies have demonstrated a high prevalence of preclinical CHF, including approximately equal numbers of people with diastolic dysfunction and systolic dysfunction. Besides CHF, a number of other causes of pulmonary venous hypertension result in increased pulmonary capillary pressure and dyspnea. Mitral stenosis is the most important. Copyright © 2020. Wolters Kluwer Health. All rights reserved. Airway Obstruction Airway obstruction at any level of the respiratory tract can lead to difficulty breathing. Tracheal stenosis resulting from intrinsic disease or extrinsic compression is characterized by dyspnea in conjunction with stridor and inspiratory retraction of the supraclavicular space. Chronic obstructive pulmonary disease (see Chapter 47) is the leading cause of airway obstruction. Chronic bronchitis is a subcategory of COPD that is defined as cough and sputum production persisting for 3 months or more in 2 consecutive years. Characteristically, these patients have a long history of smoking, productive cough, and a slowly progressive decline in exercise capacity. In advanced stages, they may become plethoric and cyanotic and cough incessantly; the term “blue bloater” has been applied to such patients. Tobacco-stained fingers, wheezes, coarse rales, rhonchi, and a prolonged expiratory phase of respiration are often present on examination. Signs of cor pulmonale (right ventricular heave, jugular venous distention, leg edema) are late findings indicative of severe, advanced disease. Another group of COPD patients are those with emphysema. Sputum production is minimal compared with that in patients with bronchitis, and mismatching of ventilation and perfusion is less pronounced; consequently, hypoxia and cyanosis are less prominent. Gradual deterioration in exercise capacity takes place over many years. Patients with advanced emphysema appear thin and barrel chested. They may purse their lips during expiration to keep their poorly supported airways from collapsing. The chest is hyperresonant, breath sounds are distant, and a few end-expiratory wheezes may be noted; expiration is prolonged. Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. Patients with COPD and bronchiectasis have a clinical presentation similar to that of patients with chronic bronchitis, except that their physical findings are more localized, the clinical course is punctuated by more frequent episodes of pneumonia, and their sputum tends to be more copious and sometimes bloody. Asthma is another of the obstructive airway diseases. It usually produces attacks of acute dyspnea, but airway obstruction may persist for a prolonged period after an acute episode and result in more chronic respiratory complaints, including exercise intolerance, cough, and sputum production. At times, sputum production may be the predominant early symptom and mistaken for infection. Diffuse wheezes are commonly noted on examination; severe cases are characterized by the use of accessory muscles, retraction, and pulsus paradoxus. Exercise-induced asthma is common in young people and may contribute to recurrent dyspneic episodes (see Chapter 48). Diffuse Interstitial Lung Disease Diffuse interstitial lung disease alters pulmonary compliance and may lead to a disturbance in the balance between ventilation and perfusion. The process is usually very gradual, and often patients have few symptoms when pulmonary involvement is mild or even moderate; however, tachypnea and cyanosis ensue in severe cases. Diffuse, “dry” midexpiratory crackles are often heard on auscultation. As the interstitial process progresses, dyspnea and hypoxia worsen and exercise tolerance deteriorates (see Chapter 51). Kyphoscoliosis Kyphoscoliosis is the major chest wall deformity capable of seriously impairing pulmonary musculoskeletal mechanics. Advanced cases can even terminate in cor pulmonale and respiratory failure. With the increase in prevalence of obesity in the United States, it has become one of the more common causes of dyspnea even in the absence of pulmonary disease. Other extrapulmonary conditions hindering lung mechanics are marked ascites (see Chapter 71) and large pleural effusions (see Chapter 43). Dyspnea is often the chief complaint in such patients. Copyright © 2020. Wolters Kluwer Health. All rights reserved. Pulmonary Hypertension Pulmonary hypertension is a serious cause of chronic dyspnea and has a poor prognosis. It may be primary or secondary and is characterized by a fixed elevation in pulmonary artery pressure and resultant strain on the right side of the heart strain. Common physical findings include an accentuated pulmonic component of S2, a right ventricular S3, the murmur of tricuspid regurgitation, and peripheral edema. Secondary pulmonary hypertension occurs with conditions that chronically elevate pulmonary artery pressure, such as recurrent pulmonary embolization, chronic hypoxemia, pulmonary parenchymal disease, and left-sided heart failure. Some forms of secondary disease have subtle presentations and can easily be mistaken for primary disease. For Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. example, pulmonary hypertension resulting from recurrent pulmonary embolization typically occurs in patients with few symptoms of embolization. Except for recalling perhaps a single episode of pleuritic chest pain and acute dyspnea, most patients report few symptoms before the onset of pulmonary hypertension. In those with symptomatic, recurrent embolization, significant pulmonary hypertension rarely develops. The reason for this paradox is unclear. The source of emboli is believed to be the proximal deep veins of the legs. Primary pulmonary hypertension is a diagnosis of exclusion. It occurs most commonly in women between the ages of 20 and 40 years. The mean age is about 35 years, and the ratio of women to men is 1.7:1. Dyspnea is the most frequently reported symptom, followed by fatigue, near-syncope, and Raynaud phenomenon. An immunologic basis for the condition is suspected because of the high frequency of antinuclear antibody seropositivity in many of these patients, especially women. Immunologically mediated endothelial damage is postulated. Hyperventilation may result and be mistakenly attributed to anxiety. Anxiety Anxiety attacks are often confused with more serious conditions because the patient may appear to be in severe respiratory distress. Patients often report chest tightness or claim that they cannot take in enough air. The florid, acute case is represented by the hyperventilation syndrome (see Chapter 226), but more common is a less dramatic, chronic feeling of dyspnea and fatigue that is affected little by exertion. Frequent sighing, multiple bodily complaints, nervousness, and normal physical examination findings are typical of such patients. Deconditioning Copyright © 2020. Wolters Kluwer Health. All rights reserved. Patients with cardiopulmonary disease often limit their physical functioning, with the resulting sedentary state creating deconditioning and worsening the effects of dyspnea on exertion. Skeletal muscle atrophy is a common finding among patients with either COPD or CHF and has been linked to low-level systemic inflammation and oxidative stress. The muscle atrophy and sedentary behavior combine to create a vicious cycle of declining function in the setting of increasing dyspnea. DIFFERENTIAL DIAGNOSIS (1–4,8,10) The causes of chronic dyspnea encountered in the office setting are listed in Table 40-1. Table 40-1 Common Causes of Chronic Dyspnea Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. Copyright © 2020. Wolters Kluwer Health. All rights reserved. WORKUP (1–4,8,10,12–32) History History remains the most useful diagnostic modality. In studies of dyspnea, the diagnosis is established by the history in about 75% of instances. However, differentiating dyspnea caused by cardiac disease from that caused by pulmonary pathology can be a challenge. For example, exertional dyspnea occurs in both cardiac and pulmonary disease. A frequent misconception is that paroxysmal nocturnal dyspnea is unique to heart failure. Excessive airway secretions from chronic obstructive lung disease often pool at night and lead to airway Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. obstruction, causing dyspnea and forcing the patient to sit up to clear the airway. Wheezing is a nonspecific manifestation of large-airway bronchospasm, whether it is caused by heart failure or obstructive lung disease. In general, a history dominated by chronic cough, sputum production, recurrent respiratory infection, occupational exposure, or heavy smoking suggests lung disease rather than a cardiac origin. However, unless a strong history of previous lung disease or substantial sputum production is present, it may be very hard to distinguish a cardiac from a pulmonary source on the basis of history alone. Moreover, as noted, both may coexist concurrently. Physical findings and laboratory studies are often necessary for a better differentiation (see later discussion). Dyspnea that is a manifestation of a chronic anxiety state may superficially mimic cardiopulmonary disease and cause some confusion. Onset at rest in conjunction with a sense of chest tightness, suffocation, and inability to take in air are characteristic features of the history. In addition, little evidence of significant heart or lung disease is present, although the patient may fear it greatly. Multiple bodily complaints, a history of emotional difficulties, an absence of activity limitations, and a lack of exacerbation on exercising argue for a psychogenic cause. Unfortunately, patients with pulmonary hypertension may have episodes that can resemble anxiety-induced bouts of dyspnea; sometimes, a young patient with primary pulmonary hypertension is incorrectly labeled “neurotic.” It is helpful to define as precisely as possible the degree of activity that precipitates the sensation of dyspnea, estimate the severity of disease, determine the extent of disability, and detect changes over time. One means of achieving these objectives is to relate symptoms to the patient’s daily activities and interpret the degree of restriction in terms of the expected endurance of a patient of similar age. Copyright © 2020. Wolters Kluwer Health. All rights reserved. Factors that may contribute to the occurrence or worsening of dyspnea should be documented, including cigarette smoking, occupational exposure, excessive salt intake, weight gain, and increasing sputum production. The occupational history is particularly important because the relationships between exposures and lung disease are becoming increasingly evident (see Chapter 39). The patient should be asked about hemoptysis; the symptom raises the possibilities of bronchiectasis, endobronchial malignancy, embolization with infarction, and pneumonia. If embolization is suspected, the physician must inquire about pleuritic chest pain, leg edema, and other symptoms of deep vein thrombosis (see Chapter 22) in addition to such risk factors as chronic venous insufficiency, inactivity, and—in young women—the use of oral contraceptives and pregnancy. Careful inquiry for historical evidence of recurrent pulmonary embolization is particularly important if pulmonary hypertension is encountered. Physical Examination Physical examination should begin with a check for tachycardia, tachypnea, fever, and hypertension. Weight increase must not be forgotten, for it may be an early sign of worsening CHF (see Chapter 32). The patient’s respiratory efforts need to be observed carefully to Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. obtain an estimate of the amount of work expended in breathing; contractions of the accessory muscles of respiration suggest severe difficulty. Retraction of the supraclavicular fossa implies tracheal stenosis that has become critical. Pursed-lip breathing and a prolonged expiratory phase are signs of significant outflow obstruction. The best way to observe air flow obstruction is to have the patient take a deep breath and blow out as hard and as fast as possible. The chest is examined for increased anterior–posterior diameter (suggestive of COPD) and deformity resulting from kyphoscoliosis or ankylosing spondylitis. Retraction of the intercostal muscles on inspiration is characteristic of emphysema. The chest should be percussed for dullness and hyperresonance and auscultated for wheezes, crackles, and quality of breath sounds. Unfortunately, eliciting wheezing on maximal forced exhalation has proved neither sensitive nor specific for the diagnosis of asthma and cannot be recommended as a technique for uncovering underlying airway hyperreactivity. Coarse crackles, heard in early inspiration and throughout expiration, suggest fluid in the airway, as occurs with bronchitis, pneumonitis, and CHF. Fine crackles, heard on mid-to-late inspiration, only occasionally on expiration, and unaffected by cough, are unrelated to airway secretions and indicative of interstitial lung disease; they may be present before x-ray changes become evident. Normal findings on lung examination do not rule out pulmonary pathology but do lessen its probability and the likelihood that it is severe. The cardiac examination should focus on signs of left-sided heart failure (see Chapter 32), detection of left-sided heart murmurs (see Chapters 21 and 33), and signs of pulmonary hypertension and its consequences (accentuated and delayed pulmonic valve component of S2, right ventricular heave, right ventricular S3, right-sided holosystolic regurgitant murmur of tricuspid insufficiency, jugular venous distention, and peripheral edema). It is important to recognize that many of the signs of right-sided heart failure may be a consequence of longstanding pulmonary disease and therefore are not specific for a cardiac etiology. The abdomen is examined for ascites and hepatojugular reflux; the legs are checked for edema and other signs of phlebitis (see Chapters 16 and 30). Finally, the patient’s mental status is checked for manifestations of an anxiety disorder; particularly germane is excessive sighing. Copyright © 2020. Wolters Kluwer Health. All rights reserved. Laboratory Studies Chest X-Ray The chest radiograph is essential to evaluation and should be studied for pulmonary venous redistribution, effusions, interstitial changes, hyperinflation, infiltrates, enlargement of the pulmonary arteries (indicative of pulmonary hypertension), cardiac chamber enlargement, and valve calcification. Upper zone redistribution of pulmonary blood flow is among the earliest radiographic findings of CHF (see Chapter 32); however, redistribution may also occur in COPD because of destruction of vessels in the lower lung fields. The radiographic diagnosis can be made with a high degree of accuracy if any two of the following criteria are met: depression and flattening of the diaphragm with blunting of the costophrenic angles on Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. posterior–anterior film; irregular lucency of the lung fields; abnormally enlarged retrosternal space; and diaphragmatic flattening or concavity on the lateral film. Chest radiography is sometimes useful for the detection of interstitial lung disease because physical findings may be minimal; however, radiographic findings may be unimpressive or very subtle, necessitating more detailed imaging by computed tomography. High-Resolution Computed Tomography Chest computed tomography (CT) may be helpful when the etiology is unclear after chest xray or when signs or symptoms point in the direction of a chronic process such as interstitial lung disease (see Chapter 51), malignancy (see Chapter 53), or chronic infection (see Chapter 52). Sputum Stains, Culture, and Cytology When an infiltrate is present, Gram stains of the sputum and culture are often informative, especially when the patient is febrile, is coughing more than usual, or reports a change in sputum. Sputum cytology is indicated under similar circumstances, particularly if hemoptysis has developed. A Ziehl-Neelsen stain for acid-fast bacilli and sputum culture for tuberculosis are also important components of the workup when an infiltrate is detected (see Chapter 49). Copyright © 2020. Wolters Kluwer Health. All rights reserved. Pulmonary Function Tests Simple pulmonary function tests can be reliably performed in the office on an inexpensive spirometer. Forced expiratory volume in 1 second (FEV1) and vital capacity are the most informative of these measurements for detecting obstructive and restrictive defects and determining their severity. The ratio of FEV1 to vital capacity is markedly reduced in clinically important obstructive disease. In restrictive disease, the ratio is close to 1.0, but the vital capacity is significantly reduced. An FEV1 determination can also provide prognostic information. A reading of less than 1.0 L/s is associated with a poor 5-year survival rate among patients with COPD (see Chapter 47). Patients suspected of having tracheal stenosis may require flow-volume studies to identify the lesion and determine its severity; referral is indicated. Assessment of Oxygenation—Pulse Oximetry, Arterial Blood Gas Pulse oximetry is a convenient, noninvasive approach to determination of arterial oxyhemoglobin saturation and of desaturation with exercise that can be useful in decisionmaking. Accuracy of most oximeters is limited to ±4% of the actual oxygen saturation. Accuracy is especially a problem at levels below 88%. Accuracy may be lower in patients with darker skin or poor peripheral perfusion due to heart failure. Oximetry will overestimate Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. oxygen saturation among heavy smokers with high carboxyhemoglobin levels. A significant desaturation during exercise measured with continuous pulse oximetry, defined as a decrease of greater than 4%, should be confirmed with arterial blood gas determinations. Arterial blood gas determinations are not routinely available in most office settings, but they are worth obtaining when deteriorating ventilation is suspected. Hospitalization should be considered when the carbon dioxide tension (PCO2) is inappropriately elevated for the respiratory rate and repeated determinations reveal further increases in PCO2. Measuring arterial blood gases before and after exercise is helpful in assessing the severity of diffuse interstitial disease. A fall in oxygen tension is evidence of a significant degree of interstitial disease. When use of accessory muscles is noted and the patient’s condition appears to be worsening, prompt hospital admission should be arranged without time taken to determine arterial blood gases in the office. Diffusing Capacity A reduction in single-breath carbon monoxide diffusing capacity may be the earliest sign of interstitial fibrosis. The test is particularly useful in the evaluation of dyspnea associated with suspected occupational interstitial disease (see Chapters 39 and 46). Abnormal rest oximetry and further desaturation with exercise would be expected. Other Tests for Heart Failure: Cardiac Ultrasound, B-Type Natriuretic Peptide Sometimes, the combination of history, physical examination, and chest x-ray proves insufficient to distinguish between heart failure and lung disease as the cause of chronic dyspnea. For additional evidence of heart failure, clinicians have turned to cardiac ultrasound and B-type natriuretic peptide (BNP). Copyright © 2020. Wolters Kluwer Health. All rights reserved. Cardiac Ultrasound Transthoracic cardiac ultrasound examination in conjunction with Doppler flow study provides a readily available, noninvasive means of detecting heart failure, be it systolic (with reduced ejection fraction) or diastolic (with evidence of impaired diastolic filling and preserved ejection fraction—see Chapter 32). In addition, it can provide evidence of pulmonary hypertension, valvular disease (see Chapter 33), and cardiomyopathy (see Appendix Chapter 33). B-Type Natriuretic Peptide BNP and the other circulating forms of natriuretic peptides—its precursor proBNP and the Nterminal peptides of proBNP designated NT-proBNP—increase in response to left ventricular wall distention and heightened cardiac pressures, common manifestations of heart failure. Natriuretic peptide determinations have been studied in the emergency room setting to help rapidly differentiate heart failure from other causes of acute dyspnea. Using a cutoff level of Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. 100 pg/mL, BNP has demonstrated a sensitivity of 90% and a specificity of 76%, producing a positive predictive value in this population of roughly 80% and a negative predictive value of 90%. Age and reduced renal function cause elevations in natriuretic peptide levels. BNP measurements have been made in community settings to screen for preclinical systolic and diastolic dysfunction but have produced unacceptably high false-positive rates with need for further extensive evaluation. In some small studies, it has effectively differentiated diastolic dysfunction from pulmonary disease as a cause of dyspnea. Neither the role of natriuretic peptide testing in patients with subacute or chronic dyspnea nor the value of other uses in the nonacute primary care setting have been fully defined. Meta-analysis of use in the emergency room setting finds modest decrease in length of stay, but no effect on admission rate or hospital mortality. Exercise Testing The neurotic patient with anxiety-induced dyspnea often benefits from undergoing chest radiography and simple pulmonary function testing; the confirmation of a well-functioning respiratory system may provide some reassurance and lessen concern over bodily symptoms. At times, a walk with the patient up and down a few flights of stairs is just as convincing for both physician and patient. Climbing stairs with a patient complaining of dyspnea is also useful if cardiopulmonary disease is suspected because exercise tolerance can be quantified in terms of the number of flights climbed and the heart and respiratory rates attained. The 6minute walk test is commonly used to assess exercise capacity in patients with COPD; simple distance is usually measured, although the product of distance times body weight has been advocated as having a more solid physiologic foundation. In the very rare cases in which there is no apparent cause after a thorough evaluation or when it is difficult to ascertain the contribution to symptoms made by more than one condition, cardiopulmonary exercise testing may be indicated. Measurement of blood pressure, heart rate, ventilation, oxygen saturation, oxygen uptake, and carbon dioxide output allow for the quantification of cardiac function, pulmonary gas exchange, and physical fitness. Copyright © 2020. Wolters Kluwer Health. All rights reserved. Evaluation of Pulmonary Hypertension Finding evidence suggestive of pulmonary hypertension (dyspnea, signs of right-sided heart strain on physical examination and electrocardiogram, prominent main pulmonary artery and hilar vessels in conjunction with decreased peripheral vessels on chest x-ray film) necessitates consideration of its treatable causes, such as recurrent pulmonary embolization, sleep apnea (see Chapter 46), and mitral stenosis (see Chapter 33). Although pulmonary hypertension is typically quite advanced by the time the diagnosis is made, efforts at earlier recognition and identification of treatable causes are imperative if the prognosis is to be improved. Echocardiography has shown considerable promise in the noninvasive diagnosis of cor pulmonale and pulmonary hypertension and their antecedent conditions. The perfusion lung scan is a safe, noninvasive means of screening for recurrent pulmonary embolization and Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. differentiating it from primary pulmonary hypertensive disease. In primary disease, the scan findings may be normal, or the scan may show a subsegmental or diffuse patchy, peripheral distribution of labeled albumin. In secondary disease resulting from recurrent pulmonary emboli, the scan shows multiple segmental or large subsegmental defects. More recently, use of chest computed tomography has replaced perfusion scanning in many settings, although it must be kept in mind that its sensitivity is limited for small peripheral emboli. A sleep study (see Chapter 46) can help confirm suspected sleep apnea as the cause of pulmonary hypertension. Elevated natriuretic peptide levels (e.g., BNP > 180 pg/mL) have been found to correlate with prognosis of pulmonary hypertension. Functional assessment can be performed by a 6-minute walking test. Cardiac catheterization is reserved for patients suspected of pulmonary artery hypertension, especially if treatment directed at lowering pulmonary artery pressure is being contemplated. SYMPTOMATIC MANAGEMENT AND PATIENT EDUCATION (33–39) The relief of dyspnea requires attention to exacerbating factors in addition to the underlying etiology. Symptomatic management begins with correcting reversible forms of airway obstruction (see Chapters 47 and 48) and precipitants of left ventricular dysfunction (see Chapter 32). Any concurrent respiratory tract infection requires treatment (see Chapter 52). If a large pleural effusion (see Chapter 43), a severe anemia (see Chapter 82), or an acute situational stress (see Chapter 226) is present, it too should receive prompt attention. Environmental irritants ought to be eliminated (see Chapter 39). All patients with dyspnea should be advised to stop smoking; often, the onset of even mild dyspnea is a sufficient stimulus to quit, especially when combined with the physician’s urging (see Chapter 54). Copyright © 2020. Wolters Kluwer Health. All rights reserved. Need for attention to the underlying cause cannot be overemphasized, whether it is heart disease (see Chapters 30, 32, and 33), lung disease (see Chapters 47, 48, and 52), a mechanical factor such as massive obesity (see Chapter 235), or an anxiety disorder (see Chapter 226). Dyspneic patients with such disorders greatly appreciate knowing the cause of their discomfort and its prognosis, especially when it differs from what their perception has been. Many patients with chronic dyspnea request home oxygen therapy. Such requests are reasonable if the patient has a condition causing chronic hypoxemia, provided that no evidence of carbon dioxide retention, with its attendant risk of suppression of respiratory drive, is present. Patients without significant hypoxemia—even those with chronic emphysema—do not benefit from oxygen therapy. Selected patients with lung or heart disease may benefit from an exercise program; exercise tolerance often improves with even modest reversals in deconditioning, although the effect on survival is unproven (see Chapters 18, 30, 31, and 47). It is important that patients be reminded to note the level of activity that they can tolerate and report any decrease. Precipitants of worsening exercise tolerance should also be monitored. Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. Patients with catheterization-proven pulmonary artery hypertension may be candidates for vasodilator therapy. A positive vasodilator response during catheterization suggests benefit from calcium channel blocker therapy. Patients with modest functional impairment may be tried on a program of an oral phosphodiesterase-5 inhibitor, an endothelin receptor antagonist, or an inhaled prostacyclin. Such treatment is usually conducted under the supervision of a cardiac consultant. The use of anxiolytics is helpful only in patients whose dyspnea is a manifestation of a severe anxiety disorder. Even then, extreme caution must be exercised in the long-term use of such medications (see Chapter 226). Prescribing tranquilizers for a patient with heart or lung disease who is anxious because of trouble with breathing is more likely to exacerbate the respiratory problem than to help it. Patients with end-stage disease who continue to experience breathlessness despite a clear diagnosis and maximum therapy of the underlying etiology are not uncommon. Depression and insomnia, as well as anxiety, become part of a vicious cycle that is difficult for family and caregivers as well as patients. Opioids in low oral and parenteral doses have been shown to provide symptomatic improvement among patients for whom palliation has become the goal of care. The principal side effect is constipation. Nebulized opioids have not been found to be effective in systematic reviews. INDICATIONS ADMISSION FOR REFERRAL AND For patients with underlying heart or lung disease who experience a worsening of their chronic dyspnea, prompt hospital admission should be considered, especially if the change is rapid. It may represent acute left ventricular decompensation, ventilatory failure, or hypoxemia. Acute anxiety can superficially mimic cardiopulmonary decompensation and needs to be ruled out (see prior discussion) before hospitalization is authorized. Pulmonary consultation may be helpful in the patient with suspected pulmonary hypertension, both for design of the diagnostic assessment and for the selection of the treatment plan if a secondary cause is identified. Copyright © 2020. Wolters Kluwer Health. All rights reserved. A.H.G./A.G.M. ANNOTATED BIBLIOGRAPHY Gelbach BK, Geppert E. The pulmonary manifestations of left heart failure. Chest 2004;125:669–682. (A careful review of the pathophysiology relevant to the differential diagnostic challenges; 132 references.) Karnani NG, Reisfield GM, Wilson GR. Evaluation of chronic dyspnea. Am Fam Physician 2005;71:1529. (Effective review of dyspnea attributable to cardiac, pulmonary, and other causes.) Le Jemtel TH, Padeletti M, Jelic S. Diagnostic and therapeutic challenges in patients with coexistent chronic obstructive pulmonary disease and chronic heart failure. J Am Coll Cardiol 2007;49:171. (Focuses on overlap in presentation, on chronic obstructive pulmonary disease [COPD] as a cardiovascular risk, and on the functional effect of skeletal muscle atrophy common to both conditions.) McLaughlin VV, Archer SL, Badesch DB, et al.; for the ACCF/AHA. ACCF/AHA 2009 expert consensus document on Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. Copyright © 2020. Wolters Kluwer Health. All rights reserved. pulmonary hypertension. Circulation 2009;119:2250. (Comprehensive, evidence-based recommendations.) Redfield MM, Jacobsen SJ, Burnett JC Jr, et al. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA 2003;289:194. (Documents high prevalences of subclinical systolic and diastolic dysfunction, with the latter associated with marked increases in all-cause mortality.) Rich S, Dantzker DR, Ayers SM, et al. Primary pulmonary hypertension: a national prospective study. Ann Intern Med 1987;107:216. (Findings from a national registry; the best available data on clinical and epidemiologic features.) Rich S, Levitsky S, Brundage BH. Pulmonary hypertension from chronic pulmonary embolism. Ann Intern Med 1988;108:425. (A review exploring the often-confusing relationship between these two conditions; 87 references.) Shah SJ. Pulmonary hypertension. JAMA 2012;308:1366. (Excellent case-based review for the generalist reader.) Sin DD, Jones RL, Man SF. Obesity is a risk factor for dyspnea but not for airflow obstruction. Arch Intern Med 2002;162:1477. (Dyspnea without objective evidence of obstruction contributes to overdiagnosis of asthma and overuse of bronchodilators among the obese.) Tobin MJ. Dyspnea: pathophysiologic basis, clinical presentation, and management. Arch Intern Med 1990;150:1604. (Useful review, with emphasis on pathophysiology; includes a good discussion of hyperventilation syndrome; 97 references.) Wang TJ, Levy D, Benjamin EJ, et al. The epidemiology of “asymptomatic” left ventricular systolic dysfunction: implications for screening. Ann Intern Med 2003;138:907. (Prevalence was 3% to 6%, but there was insufficient evidence to justify screening with echocardiography or β-type natriuretic peptide [BNP]). American Association for Respiratory Care. Exercise testing for evaluation of hypoxemia and/or desaturation: 2001 revision and update. Respir Care 2001;46:514. (Guidelines for the use of exercise testing for diagnosing causes of dyspnea and monitoring oxygen therapy; 74 references.) Bohadana A, Izbicki F, Kraman SS. Fundamentals of lung auscultation. N Engl J Med 2014;370:744. (Essential reading; all you need to know about lung auscultation; 31 refs.) Baumstark A, Swensson RG, Hessel SJ, et al. Evaluating the radiographic assessment of pulmonary venous hypertension in chronic heart disease. AJR Am J Roentgenol 1984;142:877. (Suggests that the assessment can be quite accurate, with a sensitivity of 0.75 and a specificity of 0.88.) Boxt LM, Bettmann MA, Gomes AS, et al. Shortness of breath—suspected cardiac origin. American College of Radiology. ACR appropriateness criteria. Radiology 2000;215(Suppl):23. (Rates the value of imaging tests, with standard chest x-ray coming out on top.) Cabanes L, Richaud-Thiriez B, Fulla Y, et al. Brain natriuretic peptide blood levels in the differential diagnosis of dyspnea. Chest 2001;120:2047. (BNP levels distinguished between patients with COPD and questionable diastolic dysfunction in this small study.) Carter R, Holiday DB, Nwasuruba C, et al. 6-Minute walk work for assessment of functional capacity in patients with COPD. Chest 2003;123:1408. (Simply suggests the use of distance multiplied by body weight rather that distance alone.) Come PC. Echocardiographic recognition of pulmonary arterial disease and determination of its cause. Am J Med 1988;84:384. (Provides evidence for the utility of ultrasonography in the identification and differential diagnosis of pulmonary hypertension.) D’Alonzo GE, Bower JS, Dantzker DR. Differentiation of patients with primary and thromboembolic pulmonary hypertension. Chest 1984;85:457. (The pattern on perfusion lung scan is different.) Evans SE, Scanlon PD. Current practice in pulmonary function testing. Mayo Clin Proc 2003;78:758. (Effective review.) Ferguson GT, Enright PL, Buist AS, et al. Office spirometry for lung health assessment in adults: a consensus statement from the National Lung Health Education Program. Chest 2000;117:1146. (Recommends widespread use of office spirometry of smokers in the primary care office.) Hankinson JL, Odencrantz JR, Fedan KB. Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med 1999;159:179. (Major population study.) Jones NL. Exercise testing in pulmonary evaluation: clinical application. N Engl J Med 1975;293:647. (Describes the use of exercise pulmonary function tests in evaluating dyspnea; the article on p. 341 of this issue details methods and physiology of exercise testing.) King DK, Thompson BT, Johnson DC. Wheezing on maximal forced exhalation in the diagnosis of atypical asthma. Ann Intern Med 1989;110;451. (Wheezing proved neither sensitive nor specific.) Lam LL, Cameron PA, Schneider HG, et al. Meta-analysis: Effect of B-type natriuretic peptide testing on clinical outcomes in patients with acute dyspnea in the emergency setting. Ann Intern Med 2010;153:728. (Reduced hospital stay by about 1 day possibly admission rate, but no effect on mortality.) Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002;347:61. (In the emergency room, BNP with a cutoff of 100 pg/mL had a sensitivity of 90% and a specificity of 76% for congestive heart failure as etiology of acute dyspnea.) Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02. Copyright © 2020. Wolters Kluwer Health. All rights reserved. Mulrow CD, Lucey CR, Farnett LE. Discriminating causes of dyspnea through clinical examination. J Gen Intern Med 1993;8:383. (The accuracy of clinical assessment was 70%.) Pratt PC. Role of conventional chest radiography in diagnosis and exclusion of emphysema. Am J Med 1987;82:998. (A review arguing that a high degree of accuracy can be achieved if validated criteria are used; 40 references.) Raffin TA. Indications for arterial blood gas analysis. Ann Intern Med 1986;105:390. (A critical review of uses of blood gas determinations; 76 references.) Schneider H-G, Lam L, Lokuge A, et al. B-type natriuretic peptide testing, clinical outcomes, and health services use in emergency department patients with dyspnea: a randomized trial. Ann Intern Med 2009;150:365. (No effect found on clinical outcomes or use of health services.) Schoepf UJ, Goldhaber SZ, Costello P. Spiral computed tomography for acute pulmonary embolism. Circulation 2004;109:2160. (Detailed review of comparative advantages and disadvantages of computed tomography and older imaging approaches.) Vasan RS, Benjamin EJ, Larson MG, et al. Plasma natriuretic peptides for community screening for left ventricular hypertrophy and systolic dysfunction: the Framingham Heart Study. JAMA 2002;288:1252. (Finds limited usefulness in screening.) Abernathy AP, Currow DC, Frith P, et al. Randomised, double blind, placebo controlled crossover trial of sustained release morphine for the management of refractory dyspnea. BMJ 2003;327:1. (Significant palliation among COPD patients with 20 mg of sustained-release morphine per day.) Booth S, Kelly MJ, Cox NP, et al. Does oxygen help dyspnea in patients with cancer? Am J Respir Crit Care Med 1996;153:1515. (Oxygen and air were equally effective in reducing dyspnea in this randomized, controlled trial.) Crockett AJ, Cranston JM, Antic N. Domiciliary oxygen for interstitial lung disease (Cochrane review). In: The Cochrane library, Issue 4. Oxford: Update Software, 2003. (The single trial in this review did not show an effect on mortality.) Crockett AJ, Cranston JM, Moss JR, et al. Domiciliary oxygen for chronic obstructive pulmonary disease (Cochrane review). In: Cochrane library, Issue 4. Oxford: Update Software, 2003. (Long-term oxygen therapy improved survival for patients with severe hypoxemia but not for those with moderate hypoxemia or with only arterial desaturation at night.) Jennings AL, Davies AN, Higgins JPT, et al. Opioids for the palliation of breathlessness in terminal illness (Cochrane review). In: The Cochrane library, Issue 3. Oxford: Update Software, 2003. (There was some evidence to support the use of oral or parenteral opioids but not nebulized forms.) Liss HP, Grant BJB. The effect of nasal flow on breathlessness in patients with chronic obstructive lung disease. Am Rev Respir Dis 1988;137:1285. (Nasal cannular delivery of room air provided as much relief of dyspnea as did cannular delivery of oxygen.) Man GCW, Hsu K, Sproule BJ. Effect of alprazolam on exercise and dyspnea in patients with chronic obstructive lung disease. Chest 1986;90:832. (No benefit was found in patients who had normal oxygen tension values.) Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 12:17:02.