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Shortness of Breath Christopher Taggart, MD St. Mary’s Medical Center, Department of Family Shortness of breath: Looking Medicine, Grand Junction, Colo beyond the usual suspects christopher.taggart@ sclhs.net COPD and pneumonia come to mind when a patient The authors reported no potential conflict of interest is short of breath. But the signs and symptoms detailed relevant to this article. here should lead you to suspect an uncommon cause. CASE u Joan C is a 68-year-old woman who presents to the of- PRACTICE RECOMMENDATIONS fice complaining of an enlarging left chest wall mass that ap- peared within the past month. She was treated for small-cell ❯ Consider diagnoses other lung cancer 11 years ago. She has a 45 pack-year smoking his- than asthma, COPD, heart failure, and pneumonia in tory (she quit when she received the diagnosis) and has heart patients with persistent or failure, which is controlled. Your examination reveals a large progressive dyspnea. C (5 cm) firm mass on her left chest wall. There is no erythema or tenderness. She has no other complaints. You recommend surgi- ❯ Avoid steroids in patients with acute pericarditis cal biopsy and refer her to surgery. because research shows Ms. C returns to your office several days later complaining that they increase the of new and worsening shortness of breath with exertion that be- risk of recurrence. B gan the previous day. The presentation is similar to prior asthma exacerbation episodes. She denies any cough, fever, chest pain, ❯ Consider anticoagulation with warfarin in patients with symptoms at rest, or hemoptysis. On exam she appears comfort- pulmonary arterial hyperten- able and not in any acute distress. You refill her albuterol. sion and cor pulmonale. Evi- The next day you learn that she is being admitted to the dence shows that it improves hospital with respiratory distress. An x-ray of her chest shows a survival and quality of life. A concerning mass in her right upper lung. Strength of recommendation (SOR) yspnea is an uncomfortable awareness of breath- A Good-quality patient-oriented evidence ing that occurs when complex neurochemical path- B Inconsistent or limited-quality ways used to maintain oxygenation and ventilation patient-oriented evidence D are disrupted. (See "The variable, and subjective, process of Consensus, usual practice, C 1-5 opinion, disease-oriented dyspnea" on page 528). Sometimes described as air hunger, evidence, case series increased work of breathing, chest tightness, or chest constric- tion, the symptom is usually disproportionate to the patient’s level of exertion. Most of the time dyspnea is due to either a primary lung or cardiovascular problem such as chronic obstructive pul- monary disease (COPD), asthma, pulmonary embolism (PE), pneumonia, congestive heart failure (CHF), or myocardial in- farction. However, many other illnesses can also produce this symptom (TABLE 1). This article will review the uncommon eti- ologies of dyspnea that should be considered when the usual suspects have been eliminated. 526 THE JOURNAL OF FAMILY PRACTICE | AUGUST 2016 | VOL 65, NO 8 Cardiovascular culprits trapezius that is relieved by leaning Dyspnea is a common symptom with car- forward diovascular diseases because cardiac output • pericardial friction rub relates directly to tissue oxygenation. Any pa- • electrocardiographic changes show- thology that decreases the ability of the heart ing ST segment elevation in all leads and blood vessels to transport oxygen will like- but aVR and V1 and diffuse PR interval ly trigger discord between the central, periph- depression eral, and neurochemical respiratory centers. • pericardial effusion on Two uncommon cardiovascular etiologies of echocardiography. dyspnea are pericarditis and myocarditis. ❚ Treatment. Treat non-severe and non- Pericarditis life threatening pericarditis with nonsteroi- Pericarditis is generally a self-limited con- dal anti-inflammatory drugs (NSAIDs). Avoid dition that responds promptly to initial steroids because research has shown that treatment, although it can cause significant they increase the risk for developing recur- morbidity and mortality. One study showed rent pericarditis.8 Hospitalize patients with that acute pericarditis accounted for 5% of large pericardial effusions and consider them patients presenting to the emergency depart- for pericardiocentesis. Treat cardiac tam- ment with non-ischemic chest pain.6 Another ponade with urgent pericardiocentesis and study found that the in-hospital mortality hospitalization. Suspect rate for acute pericarditis was 1.1%.7 pulmonary Pericarditis causes dyspnea by restrict- Myocarditis arterial ing the heart’s ability to relax, thus decreasing Myocarditis can have a variety of etiologies hypertension in preload and cardiac output. This occurs with (TABLE 29,10). Myocarditis causes dyspnea ei- younger patients large effusions (>20 mm in width on echo- ther by causing pericardial effusion or heart with exertional cardiography) and can lead to cardiac tam- failure. dyspnea, ponade—a medical emergency that should ❚ Diagnosis. Myocarditis can be difficult fatigue, chest be suspected in patients with muffled heart to diagnose. Suspect it in any patient with pains, or sounds, hypotension, and increased jugular cardiogenic shock, acute or subacute left ven- palpitations who venous distention (Beck’s triad). tricular dysfunction, or myocardial damage don't have other Pericarditis etiologies include: from a non-coronary artery disease source. heart or lung • infectious causes (viral and bacterial Echocardiography and cardiac serum bio- disease signs entities, myocarditis), markers can help diagnose myocarditis, but or symptoms. • rheumatologic causes (gout, systemic the diagnostic gold standard remains myo- lupus erythematosus, tumor necrosis cardial biopsy. factor receptor-associated periodic ❚ Treatment. Treatment is focused on syndrome [TRAPS], familial Mediter- 2 goals: treating the specific etiology sus- ranean fever), pected and stabilizing any hemodynamic • post-cardiac injury syndromes (either instability. Patients with mild cases can be of the acute [2-4 days post injury] or treated and monitored in the outpatient late [Dressler syndrome] variety), setting. • metabolic disorders (hypothyroid dis- Immunosuppressive therapy with im- ease, dialysis-related conditions), and munoglobulin or steroids is not routinely rec- • malignancy. ommended, but a trial may be considered in children, patients with severe hemodynamic More than 80% of pericarditis cases in compromise, or patients with giant cell arteri- developed countries are idiopathic and are tis, another autoimmune condition, sarcoid- assumed to have a viral source.8 osis, or eosinophilic or non-viral myocarditis. ❚ Diagnosis. Acute pericarditis is diag- ❚ Because of the risk of sudden death nosed when 2 or more of the following symp- from ventricular arrhythmias, any patient toms are present: with cardiac symptoms such as chest pain, • pleuritic chest pain radiating to the dyspnea, or palpitations should be admitted JFPONLINE.COM VOL 65, NO 8 | AUGUST 2016 | THE JOURNAL OF FAMILY PRACTICE 527 Pulmonary causes Shortness of breath is common with most The variable, and subjective, pulmonary diseases, although it may not process of dyspnea be an initial symptom and may have an in- sidious onset. It occurs once oxygenation of The mechanism of action of shortness of breath is a complex and blood becomes inadequate, resulting in pe- incompletely understood one that involves the central and pe- ripheral nervous system activation and neu- ripheral nervous systems and neurochemical modulators. In the rochemical dissociation. Most patients with central nervous system, the medullary respiratory center likely relays increased oxygen demand to the anterior insula. The anterior insula, a pulmonary infection, asthma exacerbation, which is where dyspnea is perceived as unpleasant, then simultane- or COPD will have dyspnea. Once infection, ously disseminates this information to the cerebral cortex and the asthma, and COPD have been ruled out, respiratory muscles to increase respiration and oxygen.1-3 other pathologic processes that interrupt oxy- genation should be considered. Unlike COPD The peripheral nervous system measures current oxygen flux and lung mechanics through pulmonary stretch mechanoreceptors, and infections, patients with lung cancer may pulmonary irritant receptors, and alveolar C fibers. Input from all not have dyspnea until the end stages of their 11 of these receptors ascends the respiratory pathway and affects how disease. The following entities should be dyspnea is perceived. For example, a patient may complain of short- considered in patients with dyspnea when ness of breath because the medullary respiratory center interprets more common causes have been eliminated. input from activated pulmonary muscular stretch receptors in the setting of discordant oxygen (measured via peripheral chemorecep- Restrictive lung diseases tors) and carbon dioxide levels (measured by medullary chemorecep- Restrictive lung disease occurs when func- 2,4,5 tors) as an increased work of breathing. tional lung volume is decreased, either by Neurochemical dissociation, which is the difference between the an intrinsic or extrinsic source. As a result, brain’s desired oxygen level and the amount it gets, is one potential these lung diseases cover a wide variety of hypothesis to explain why dyspnea is subjective and variable.2,5 One pathologies and disease processes including patient may complain of moderate or severe
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