Dyspnea, is defined by the American Thoracic Society as a subjective experience of breathing discomfort. This experience comes from interactions among various physiological, psychological, and environmental factors. Dsypnea is a symptom and it should not be confused with the increased work of breathing, which is a physical sign. In order to be reported as a symptom, a sensation should be perceived as unpleasant and felt as abnormal. Dyspnea is one of the most common complaints faced by a hospitalist.

Generally speaking, causes of dyspnea can be divided into:

  • Pulmonary (such as bronchospasm, pneumonia, pneumothorax, airway obstruction, pleural effusion, interstitial lung disease)

  • Cardiovascular (congestive heart failure, myocardial infarction, cardiac tamponade, pulmonary embolism, arrhythmias)

  • Miscellaneous (anemia, deconditioning, drugs, pregnancy, diabetic ketoacidosis, neurological, fractures, psychiatric causes, and obesity).

Discussions of all of the these etiologies are beyond the scope of this chapter. Here, we will focus on the pathologies which hospitalists come across every day. These include pneumonia, bronchospasm (chronic obstructive pulmonary disease (COPD), asthma), congestive heart failure, and pulmonary embolism (PE).

A thorough history, physical examination followed by laboratory and imaging studies usually lead to the diagnosis of the underlying etiology of dyspnea. The diagnostic approach is discussed in detail below.

In addition to obtaining general history, physicians should focus on associated cough, sputum production, hemoptysis, chest pain, wheezing, orthopnea, palpitations, abnormal weight loss, and generalized, ie. anasarca, or localized edema of the body. Patients should also be asked about acuity, severity, and frequency of their dyspneic episodes.

When evaluating a patient with shortness of breath, it is always important to consider life-threatening conditions and to stay vigilant that a heart attack, a pulmonary embolism, acutely decompensated heart failure, acute severe hypoxemia of various reasons, could happen at any time, in a hospitalized patient.

During the initial interview, all patients should be asked about their smoking history, also including the underlying second hand exposure which is usually associated with a previous similar episode.

Asthma and COPD are the most common obstructive lung diseases. Patients suffering from these conditions usually mention wheezing or chest tightness as a presenting complaint. For example, a patient with an acute bronchoconstrictive episode, may describe a sense of chest tightness, even when their lung function is preserved.

Patients with COPD have strong smoking history.

Any diseases of the chest wall, such as those which cause stiffness, such as kyphoscoliosis, or weakens the respiratory muscles, such as Guillain-Barre or myasthenia gravis, could also cause dyspnea.

Pleural effusions, whether as a stand alone diagnosis, or associated with other conditions, could also cause an increase in the work of breathing. Diseases of the lung parenchyma, such as pneumonia could also cause dyspnea.

The association of a lung infiltrate /consolidation on an imaging study (Chest X-ray or CT scan) along with symptoms such as fever, chills, productive cough, malaise, dyspnea, are suggestive of pneumonia.

Diseases of the heart or pericardium could present with dyspnea.

Hypoxemia due to intracardiac or intrapulmonary shunt, V/Q mismatch can also cause dyspnea. Diastolic dysfunction, described as a stiff left ventricle, is also associated with severe dyspnea, even with minimal physical activity, especially if it associated with other valvulopathies, such as mitral regurgitation.

Constrictive pericarditis can present with an increased of the pulmonary and intracardiac pressures, followed by dyspnea. Cardiac tamponade has a similar mechanism.

Venous thromboembolism, such as PE (pulmonary embolism) causes dyspnea. Any other pulmonary disease, such as pulmonary hypertension, ILD (interstitial lung disease), could also be associated with increased work of breathing. Physicians should be aware that shortness of breath may be the only red flag of a cardiac event, such as a myocardial infarction, tachy/brady arrhythmias.

Myocardial infarction (MI) is usually associated with chest pain but silent MI (described in elderly, women and diabetics) is also a well-known cause of dyspnea. Patients usually have underlying risk factors of MI in such cases.

Patients who suffer from anemia, could also present with anemia, especially during the high oxygen demand, such as physical activity. Overweight patients can also become breathless.

Hospitalized patients, with a prolonged length of stay, especially the elderly, may develop deconditioning, which could also manifest with breathlessness.

Generally, most dyspneic patients who present to the emergency department usually have low oxygen saturation and rapid respiratory rate, which may or may not be associated with altered mental status, excessive sweating, use of accessory muscles of respiration, and cyanosis based on severity of dyspnea.

It is important to remember that the differential diagnosis of a dyspneic patient should start with the first moment we see the dyspneic patient. An acute event could happen even in a patient who has been in the hospital for several days.

Also, when a patient becomes acutely dyspneic while sitting up, that is called platypnea, and may be a sign of hepatopulmonary syndrome.

Specific physical examination findings differ based on underlying cause. These include findings of fluid overload such as lower extremity pitting edema. Examination of the lung should include inspection, percussion, palpation and auscultation. Look for accessory muscle use, paradoxical abdominal movement, tripod positioning; these are signs of increased airway resistance. Bilateral Distant breath sounds, pulmonary rhonchi, wheezes, and prolonged expiratory phase are clues of the airways disease. Checking for the chest movement symmetry is also important.

Jugular venous distension (JVD) and S3 on cardiac exam.

In addition, clubbing may clue towards chronic hypoxemia. Anemic patients may appear pale with obvious source of bleeding (such as in trauma patients).

Patients who describe breathlessness with activity should be evaluated at the beginning and the end of ambulation. Their oxygen levels with and without supplemental oxygen, at rest and with ambulation, should be recorded.

Characteristic physical exam maneuvers which can guide towards the underlying etiology of dyspnea include hepatojugular reflux and egophony (E-A change on auscultation due to focal consolidation of pulmonary parenchyma in patients with pneumonia). Pulsus paradoxus, a greater than normal ( >10 mmHg) inspiratory decline in systolic arterial pressure can be found in cardiac tamponade, severe asthma, or other pericardial disease. Inability to lie in a supine position may also be sign of fluid overload. These physical examination findings are usually sensitive but not specific.

A series of laboratory and radiographic tests may be needed to evaluate dyspnea. According to the clinical presentation and history, complete blood count (CBC), comprehensive metabolic panel (CMP), brain natriuretic peptide (BNP), D-dimer, serial cardiac markers and 12-lead electrocardiogram (ECG), chest x-ray (CXR), lower extremity ultrasound, two-dimensional echocardiography, and ventilation/perfusion (V/Q) or computed tomography (CT) scan, should be considered.

CBC can help diagnosing underlying cause of anemia, such as leukocytosis in pulmonary infection. Physicians should be aware that the hemoglobin concentration may be normal in patients despite blood loss. Serial haemoglobin and haematocrit measurements and close monitoring of these patients for hemodynamic stability are important steps in acute blood loss.

CMP can help evaluate underlying renal and hepatic status. A good example of this would be a dyspneic patient with high creatinine and fluid overload but normal cardiac function, revealing renal failure as a cause of fluid overload and dyspnea. Elevated liver function tests (LFTs) or INR (international normalized ratio) can be due to vascular congestion.

Brain natriuretic peptide (BNP) is usually elevated in hypervolemic patients, such as in CHF or renal failure. A recent research data suggests an inverse relationship between BNP and NT-pro BNP levels and body mass index. Given the prevalence of obesity world wide, we need to understand the limitations of these heart failure biomarkers.

D-dimer is one of the more complex tests to interpret. It is used to rule out pulmonary embolism. Because it has a very high negative predictive value a negative D-dimer almost always rules out PE. However, a positive D-dimer may be due to a blood clot (PE) but may be due to numerous other clinical conditions. Literature review revealed that patients with negative D-dimer and low risk of PE should not be pursued for further testing for PE.

ECG and cardiac biomarkers, i.e. Troponins, are the first line test to evaluate cardiac ischemia, along with patient’s clinical presentation and risk factors.

It is important to know that a normal ECG does not rule out non-systolic time elevation myocardial infarction (NSTEMI) (NSTEMI) or unstable angina, which can be a cause of dyspnoea. Also, the first set of cardiac biomarkers are neither sensitive nor specific in cases of acute MI. ECG can also give clues regarding pericardial tamponade (electrical alterenans) and pulmonary embolism (right-sided strain pattern).

Chest x-ray is essential to evaluate dyspnea. Findings such as interstitial edema, pleural effusion and dilated cardiac shadow (in cases of fluid overload), consolidation (such as in pneumonia and aspiration), pleural effusion (in CHF or pneumonia), discrete loss of vascular markings (in pneumothorax), water-bottle heart (in pericardial effusion) and hyperinflation (in COPD and asthma) can all give clues to diagnosis.

Lower extremity ultrasound can diagnose DVT (harbinger of PE). Two-dimensional echocardiography can help evaluate the cardiac function and evaluate pulmonary artery pressure. CT angiography for pulmonary embolism is another commonly used test. It should be avoided in patients with high creatinine (to prevent contrast-induced nephropathy). In such patients, a V/Q scan can be used to evaluate the probability of PE. High resolution CT is usually reserved for evaluation of interstitial lung disease.

Framingham criteria are well known for the diagnosis of congestive heart failure. Its major criteria include paroxysmal nocturnal dyspnea, neck venous distention, acute pulmonary edema, increased central venous pressure, and positive hepatojugular reflux on clinical exam. Other major criteria include rales and S3 gallop on auscultation, and cardiomegaly on imaging. Weight loss of greater than 4.5 kg in 5 days during treatment is also one of the major criteria. Minor criteria include extremity edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, decrease in vital capacity by one third from normal, and tachycardia. The sensitivity of Framingham’s score for diagnosis of congestive heart failure is almost 100%. Diagnosis of CHF needs at least two major criteria or one major criterion in conjunction with two minor criteria.

History of respiratory tract infection and pulmonary infiltrate on chest x-ray are needed for the diagnosis of pneumonia.

To make the diagnosis of bronchospasm in pulmonary disease, including asthma and COPD, pulmonary function tests (PFTs) alone are sufficient. PFTs should be used once acute exacerbation is resolved (after discharge from the hospital as outpatient study) to avoid false positive results.

No single diagnostic test can be relied on for the diagnosis of pulmonary embolism (PE). but clues such as sudden shortness of breath without any known lung pathology with hypoxemia and increased respiratory rate, non-specific chest x-ray findings, underlying hypercoagulable status, if known, or underlying active malignancy, risk factors, can all help in the diagnosis.

Given the ongoing increase in spiral CT performance in detecting pulmonary embolism, ventilation /perfusion scan although a valuable test, is being performed less often. Several images are being taken during the scan, with the rational that only the ventilation is normal in non perfused areas of lung, which is suggestive of a PE.

There are indeterminate cases, when a suspicion of a venous thromboembolism still exists. Non invasive Duplex venous US may be helpful in evaluating these cases. The Doppler US carries a sensitivity and specificity of 89% and 100% respectively in detecting DVTs.

A careful history and physical exam can hint to a possible diagnosis and further tests should be requested to confirm that particular diagnosis. Ordering irrelevant tests such as CT scan in patients with a clear-cut picture of pneumonia or lower extremity ultrasound in patients with obvious CHF exacerbation is common and should be avoided.

Emergency management of dyspnea depends on its severity. The first step is to correct, if possible, the underlying cause of the dyspnea. In cases when hypoxemia is noted at rest with a dyspneic patient, supplemental oxygen can be administered. When this method does not improve oxygenation and patients worsen, emergent intubation may precede further testing.

Always remember, stabilizing a critical patient is the most important step in the management of dyspnea.

During initial assessment, physicians should rule out etiologies like tension pneumothorax, aspiration, and cardiac tamponade as these are reversible and can be life-threatening. Other life-threatening causes that need to be kept in mind include anaphylaxis and status asthmaticus.

Once a patient is stabilized, quick assessment should be initiated to evaluate the cause of dyspnea. When a preliminary diagnosis is obtained, treatments should be initiated right away.

After following these steps, management then is dependent on the cause of dyspnea. Intravenous antibiotics should be initiated within hours of diagnosis of pneumonia. If bronchospasm is the primary diagnosis, steroid treatment should be started with beta-2 agonist breathing treatment. In patients in whom myocardial ischemia is the underlying diagnosis, ECG and cardiac enzymes should be used to evaluate it further.

The ACS (acute coronary syndrome) treatment is beyond the scope of this chapter.

Intravenous diuretics may be used in patients presenting with dyspnea secondary to acutely decompensated systolic/diastolic heart failure.

In cases of PE, anticoagulation should be started. Patients with acute, active blood loss as a cause of dyspnea should be volume resuscitated first before blood transfusion, as blood type and cross matching can be time consuming.

At the time of initial evaluation, pitfalls include failure to identify signs of respiratory failure and inability to take appropriate immediate action such as securing airway. Dyspnea can be due to a combination of multiple etiologies and concentrating on one may lead to missing another underlying etiology. Pulmonary embolism is still considered as one of the common missed diagnosis in hospitals. Finally, patients may appear well during the initial presentation but may decompensate quickly during transfer to the floor or during radiological studies.

While the work up of dyspnea is fraught with potential pitfalls we also must be careful after we initiate therapy. Unmonitored anticoagulation can lead to easy and at times life-threatening bleeding. It is important to note that increased white cell count in patients with bronchospasm can be due to steroids rather than worsening or new infection. Ceftriaxone, commonly used for community-acquired pneumonia, can lead to elevated LFTs. Tachycardia is a common side effect of albuterol. Empyema is a common complication of pneumonia and if found, needs to be drained. Failure to recognize empyema is another common pitfall in the management of pneumonia.

Simon, PM, Schwartzstein, RM, Weiss, JW. “Distinguishable types of dyspnea in patients with shortness of breath”. Am Rev Respir Dis. vol. 142. 1990. pp. 1009

Maisel, A. “B-type natriuretic peptide levels: diagnostic and prognostic in congestive heart failure: what's next”. Circulation. vol. 105. 2002. pp. 2328

Manning, HL, Schwartzstein, RM. “Pathophysiology of dyspnea”. N. Engl. J. Med. vol. 333. 1995. pp. 1547-1553.

Cowie, MR, Struthers, AD, Wood, DA. “Value of natriuretic peptides in assessment of patients with possible new heart failure in primary care”. Lancet. vol. 350. 1997. pp. 1349-53.

Wells, PS, Ginsberg, JS, Anderson, DR. “Use of a clinical model for safe management of patients with suspected pulmonary embolism”. Ann Intern Med. vol. 129. 1998. pp. 997-1005.

Sahn, SA, Heffner, JE. “Spontaneous Pneumothorax”. N Engl J Med. vol. 342. 2000. pp. 868-874.

“Harrison’s Principles of Internal Medicine”.

Madamanchi, C. “Obesity and natriuretic peptides, BNP and NT pro-BNP: mechanisms and diagnostic implications for heart failure”. Int J Cardiol. vol. 176. 2014 Oct 20. pp. 611-7.