Diagnosing and Managing Dyspnea
Dyspnea in adults—whether acute (minutes to a few days) or chronic (weeks to months or longer)—is a common diagnostic challenge, forcing the physician to be perceptive to clinical clues. One of the hallmark symptoms of lung disease, dyspnea has very low specificity, and can occur in isolation or accompany chest pain, cough, and/or hemoptysis.1,2
Making a Diagnosis
Dyspnea or shortness of breath is the subjective, uncomfortable awareness of one’s breathing. It is often confused with tachypnea, which is an increase in the respiratory rate above 12 to 16 breaths per minute. Patients will seldom volunteer that they are dyspneic unless it is acute and unrelieved by rest. How do you diagnose the condition?
• Is dyspnea acute or chronic? Ask the patient if the dyspnea began suddenly or increased in severity recently. Find out how long the shortness of breath has been occurring (ie, days, weeks, or months). In addition, take note of current medications, as well as smoking and occupational history. Lastly, ask if the patient has other symptoms in addition to dyspnea.
• Is it a preexisting condition or a new ailment? With acute dyspnea, consider whether it is related to other acute conditions, such as acute coronary syndrome, acute pulmonary embolism, acute pulmonary aspiration, acute asthma, and acute COPD exacerbation. The patient’s clinical history will help narrow the differential diagnosis. Diagnosis and the plan of care will be predicated on the patient’s symptoms and response to treatment.
• How does the dyspnea fit into the patient’s daily activities? Dyspnea needs to be interpreted and quantitated in the context of your patient’s rest, exercise, and sleep. Note: Do not immediately attribute chronic nor acute dyspnea to physical deconditioning as this will delay the diagnosis of other important and often, treatable, and potentially serious conditions. Recurrent dyspnea can be a symptom of uncontrolled asthma, acute cardiogenic or noncardiogenic pulmonary edema, acute pulmonary embolism, pulmoanry aspiration, or it can be due to paroxysmal atrial dysrhythmias (ie, atrial fibrillation or intermittent heart block).
• Does the dypnea occur in specific situations? For example, understanding whether dyspnea is worse in certain positions—ie, orthopnea (dyspnea in the recumbent position, relieved with assuming the upright position), paroxysmal nocturnal dyspnea (dyspnea that awakens the patient from sleep, relieved by the upright position), platypnea (dyspnea in the upright position, relieved with lying down), or trepopnea (dyspnea in only one lateral decubitus position, not both), which is typically found in heart failure—can help diagonse comorbidities.
Understanding Comorbidities
Dyspnea with COPD occurs primarily after walking when patients develop dynamic hyperinlation or what the authors call “acute air constipation.” COPD patients have no problems breathing air in but become exhausted from not being able to breathe completely out before the intake of the next breath of air, which is compounded by tachypnea and anxiety. Symptoms of chest tightness, not chest pain, are commonly seen in asthma and COPD exacerbations due to dynamic hyperinflation. Certain combinations of symptoms with acute dyspnea, such as cough with sputum production, can lead the physician or provider to consider a diagnosis of acute pneumonia, bronchitis, or an exacerbation of COPD.
Chronic dyspena, on the other hand, can suggest COPD, chronic pulmonary embolism, anemia, asthma, interstitial lung disease (ILD), drug-induced lung disease (eg, prednisone, amiodarone, methotrexate, antibiotics), cardiac disease, obesity, lack of physical activity, psychological depression, malignancy, and tobacco dependence that may help to narrow your differential and focus your physical examination.3
COPD and hepatopulmonary syndrome often cause platypnea. Orthopnea in a COPD patient should alert the clinician to diagnose systolic heart dysfunction. Patients with systolic heart failure often have dyspnea with exercise and at rest. Diastolic heart failure, on the other hand, typically causes dyspnea on exertion.
However, dyspnea can occur as a normal physiologic response to more exercise than the patient can tolerate. A change in the ability to tolerate exercise and/or avoidance of exercise can be a surrogate marker of dyspnea, which the patient will often fail to mention or even deny because they are not dyspneic at rest and/or adapt to their symptoms by becoming sedentary. It is important to quantify the amount of physical exertion or exercise needed to produce dyspnea.
Chest pain and dyspnea occurring acutely should always alert the clinician to a possible cardiac etiology, including acute coronary syndromes and aortic dissection, in addition to possible pneumothorax and acute pulmonary embolism. The most common symptoms in acute pulmonary embolism are dyspnea (73%), pleurisy (66%), cough (37%), and hemoptysis (13%).4
Orthopnea is associated with gastroesophageal reflux (GERD), congestive heart failure, morbid obesity, and ascites. Paroxysmal nocturnal dyspnea and trepopnea accompany orthopnea when decompensation develops. And, trepopnea is often an overlooked symptom that leads to avoiding rest or sleep in the left lateral decubitus position and gives rise to right-sided pleural effusions in decompensated heart failure.5
Laboratory Testing
The physical examination should not be neglected in favor of ordering laboratory or radiologic tests. Document the presence or absence of obesity, cachexia, wheezing, rhonchi, crackles, heart murmurs, gallops, and peripheral edema.
Careful selection of tests based on the history and physical examination may then be used to ascertain the diagnosis. In one prospective study, 85 patients with a primary complaint of chronic dyspnea were seen in a pulmonary subspecialty clinic.6 The clinic achieved 100% success in determining the causes of dyspnea versus 66% accuracy based on clinical impression alone. In this study, 75% of chronic dyspnea cases were attributed to pulmonary disorders, 10% were caused by cardiac disorders, 5% due to GERD, and 5% because of physicial deconditioning.6
Specific therapy was effective in reducing or eliminating dyspnea in the majority of cases. The authors concluded that a diagnostic approach to chronic dyspnea based on objective findings and verification, rather than clinical impression alone, will consistently lead to an accurate diagnosis and an improved therapeutic outcome..6
Testing to consider include:
• A pulse oximetry (SpO2) <90% correlates with a PaO2 <60 mm Hg under normal acid-base conditions. But normal SpO2 (>92%) does not rule out lung or heart disease as the cause of dyspnea. Oxygen saturation is neither sensitive nor specific in identifying the cause of dyspnea in patients.
• Chest x-rays are most useful tool to diagnose interstitial lung disease. CXR assesses for cardiomegaly, infiltrates (ILD, chronic pneumonia), lung hyperinflation (late sign of COPD or severe asthma), nodules or masses (lung cancer, metastatic cancer) and pleural effusions—which likely needs further evaluation with thoracentesis.
• Cardiopulmonary exercise testing (CPET)can evaluate for dyspnea due to heart, lung, and physical deconditioning.
• Office spirometryis very valuable when interpreted with flow volume loops. Obstructive disease is confirmed based on FEV1/FVC <0.70 with restrictive disease suggested by FVC <80% predicted. Upper airway obstruction can be recognized when the inspiratory limb of the flow volume loop is truncated, no longer appearing like the bottom of an chicken egg.
• A complete blood count (CBC) can confirm anemia.
• Brain natriuretic peptide (BNP) can detect left and/or right heart dysfunction. Level >100 pg/mL may be useful for the diagnosis of heart failure who present with acute dyspnea. Routine use of BNP for all patients with acute dyspnea is not recommended unless the history and physical examination warrant it.
Additional Testing
If the cause of dyspnea is not evident based on these initial tests, order additional testing within 2 weeks:
• Complete pulmonary function tests (PFTs) with lung volumes and spirometry to look for restrictive, obstructive, or mixed disease, flow volume loops to detect fixed or variable large airways obstruction, and carbon monoxide diffusing capacity (DLco) can provide very valuable information. A low DLco is nonspecific but may be due to anemia, emphysema, ILD, or pulmonary vascular disease (eg, pulmonary arterial hypertension).
• Methacholine challenge test or bronchoprovocation is most useful in detecting or eliminating asthma.
• A D-dimer test has limited utility identifying patients with low probablity for pulmonary embolism.
If the PFTs do not help lead or confirm a diagnosis, then:
• CPET to ascertain between a cardiac pulmonary etiology versus physical deconditioning. Physical deconditioning in the absence of cardiopulmonary disease can be recognized by a decrease in maximal oxygen uptake and normal blood gases. If a cardiac etiology is revealed by this study, then a cardiology referral and cardiac catheterization may be needed.
• Echocardiogram if you suspect left or right heart disease, pulmonary arterial hypertension, or pericardial effusion
If still without a diagnosis, then consider:
• Chest CT to look for ILD, emphysema, and chronic pulmonary embolism.
• Esophageal pH probe study to look for clinically silent GERD that can cause vocal cord dysfunction.
• Sinus CT to look for chronic sinusitis that can cause vocal cord dysfunction or pulmonary aspiration.
The entire evaluation of dyspnea should take less than 3 weeks to complete. Asthma, COPD, ILD, and cardiomyopathy account for two-thirds of chronic dyspnea cases, but not coronary artery disease. ■
To avoid pulmonary pitfalls in diagnosing and managing dyspnea:
1. Determine if dyspnea is acute or chronic. Acute dyspnea may be due to a
life-threatening condition—eg, acute pulmonary embolism where dyspnea is the most prominent symptom, not chest pain or hemoptysis.
2. Listen to the patient and ask how he/she sleeps to detect orthopnea,
platypnea, trepopnea, and paroxysmal nocturnal dyspnea.
3. Refrain from ascribing dyspnea to physical deconditioning alone.
4. Use the clinical history and focused physical examination to determine the need for additional testing to confirm specific diagnosis.
5. Recognize that pulmonary function testing with flow volume loops, DLco, CXR, CBC, and BNP are useful in evaluating chronic dyspnea. A D-dimer test has limited utility identifying patients with low probability for pulmonary embolism.
6. Asthma, COPD, ILD, and cardiomyopathy are the most common causes of chronic dyspnea.
References:
1. Manning HL, Schwartzetein RM. Pathophysiology of dyspnea. N Engl J Med. 1995;333(23):1547-1553.
2. Parshall MB, Schwartzstein RM, 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;185(4):435-452.
3. Pratter MR, Abouzgheib W, Akers S, et al. An algorithmic approach to chronic dyspnea. Respir Med. 2011;105(7):1014-1021.
4. Stein PD, Terrin ML, Hales CA, et al. Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-exisitng cardiac or pulmonary disease. CHEST. 1991;100(3):598-603.
5. de Araujo BS, Reichert R, Eifer DA, et al. Trepopnea may explain right-sided pleural effusion in patients with decompensated heart failure. Am J Emerg Med. 2012;30(6):925-931.
6. Pratter MR, Curley FJ, Dubois J, Irwin RS. Cause and evaluation of chronic dyspnea in a pulmonary disease clinic. Arch Intern Med. 1989;149 (10): 2277-2282