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Symptoms: Shortness of Breath, Chest Pressure

Wiler, Jennifer L. MD, MBA

doi: 10.1097/01.EEM.0000285243.34866.7c
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Dr. Wiler is the assistant chief of clinical operations in the department of emergency medicine at Washington University in St. Louis.



A 64-year-old man presents with shortness of breath. Over the past month, he has had increasing dyspnea on exertion, intermittent chest “pressure” made worse when lying flat, and mild lower extremity swelling.

He denies fevers, cough, or orthopnea. He has lost 10 pounds unintentionally, but he denies night sweats. His history is significant for “heart problems,” and a 50-pack-a-year cigarette-smoking history. His vitals are heart rate 110 bpm, respiratory rate 24 bpm, blood pressure 201/75 mm Hg, and pulse oximetry 93% on room air.

The radiograph of his chest is shown. What bedside test may help you make the diagnosis?



The pericardium is a relatively inelastic avascular structure consisting of two layers, visceral and parietal, which encase the heart. It attaches to the sternum, diaphragm, and anterior mediastinum, and invests the vena cava and great vessels, serving as the anchor of the heart in the central thorax. A pericardial effusion is defined as an abnormal amount or character of fluid within the pericardial space. Normally the pericardial space contains 15–50 ml of fluid, which serves as lubrication between the pericardial layers.



Abnormal fluid accumulation depends on the underlying etiology, and can be caused by a variety of factors, including obstructive lymphatic drainage, trauma, viral (coxsackie, hepatitis, HIV), bacterial (pneumococci, staphylococci, streptococci, Legionella, Neisseria), tuberculosis, fungal (histoplasmosis, coccidiomycosis, Candida), rickettsial (syphilis, Lyme) infections, parasitic, malignancy, uremia, myxedema, acute myocardial infarction, post-irradiation, sarcoid, collagen vascular disease (lupus, rheumatoid, scleroderma, ankylosing spondylitis, Wegener's), medication-induced (procainamide, hydralazine, isoniazid, phenytoin, anticoagulants), and idiopathic.

A pericardial effusion can be acute or chronic (more than six months' duration) and significantly influences the patient's symptomatology. The inelastic properties of the pericardium limit rapid acute cardiac dilation and enhance coordinated mechanical interactions of the cardiac chambers. (Am J Physiol 1992;262:H1725.) Yet, when subjected to chronic dilatational stress forces of a slowly accumulating pericardial effusion, the pericardium can dilate, shifting the pericardial pressure-volume relation substantially to the right, allowing an effusion to become sizeable without compressing the cardiac chambers. (Circulation 2006;113[12]:1622.) The dreaded complication of an effusion is pericardial tamponade. Rapid or significant volume accumulation in the pericardial sac can result in impaired chamber filling, shock, and ultimately death.

Symptoms are highly dependent on the rate of fluid accumulation. Rapid accumulation can cause symptoms with as little as 80 ml of fluid. Meanwhile, slow progressing effusions can grow to two liters without causing symptoms. Patients can present with chest pain, pressure, or discomfort (classically pericarditis pain is sharp; retrosternal chest pain relieved by sitting up and leaning forward and worsened when the patient is supine; JAMA 2003;289:1150). Because the pericardium is well innervated, severe pain can result from pericardial inflammation. (Circulation 2006;113[12]:1622.) Patients also present with palpitations, syncope, cough, dyspnea, or obtundation if in shock.

On examination, patients may have a widened pulse pressure, tachycardia, tachypnea, a pericardial friction rub, hepatosplenomegally, weak peripheral pulses, edema, and cyanosis. Patients with impending or early tamponade usually appear anxious, and can have the classic Beck's triad of hypotension, muffled heart sounds (especially with large effusions), and jugular venous distention. (Circulation 2006;113[12]:1622.) The hallmark of cardiac tamponade is “pulsus paradoxus” (>10 mm Hg drop in systolic arterial pressure during inspiration). (Eur Heart J 2004;25:587.)

The differential diagnosis of chest pain and pericardial effusion is vast. It includes but is not limited to myocardial infarction, pulmonary embolism, aortic dissection, constrictive pericarditis, cardiac tamponade, dilated cardiomyopathy, and cardiogenic or noncardiogenic pulmonary edema.

Evaluation and management of pericardial effusions in the emergency department depend on the patient's hemodynamic status, institutional resources, and the suspected etiology of the effusion. Evaluation may include CBC with differential (for evidence of infection or immunocompromised conditions), chemistries (identify renal failure), cardiac enzymes (can be elevated with acute pericarditis for one to two weeks), suspected underlying etiology-specific studies (Lyme-titer, RPR, anti-nuclear antibody, rheumatoid factor, thyroid studies, etc.), and electrocardiogram (classically acute pericarditis demonstrates diffuse ST segment elevations with concomitant PR depression except in aVR, although ischemia-related pericarditis may have a more anatomically distributive pattern).

Pericardiocentesis can be diagnostic and therapeutic to relieve tamponade. Analysis of the pericardial fluid is essential to define the etiology of fluid development. Pericardial fluid laboratory studies to be considered are lactic acid dehydrogenase, total protein, glucose, specific gravity calculation, gram stain, smear for acid-fast bacilli, cultures (bacterial, fungal, and viral), cell count with differential, and hematocrit for blood aspirate.

Upright chest radiographs will likely reveal an enlarged, globular cardiac silhouette and/or an epicardial fat stripe or “double lucency” sign. (JAMA 2007;297[16]:1813.) An associated pleural effusion also may be appreciated. Portable views or poor inspiration can result in false-positive findings, and radiography may be unreliable to establish a diagnosis.

Chest computerized tomography scans can reliably identify as little as 50 mL of fluid, and magnetic resonance imaging can identify as little as 30 mL of fluid. Both are helpful for loculated effusions. The standard for diagnosis, however, is echocardiography.

Bedside ultrasonography has become an essential tool to identify fluid within the pericardial sac. It is technically simple and noninvasive, and it yields clinically important information rapidly. An effusion appears as a dark echo-free strip between the visceral and parietal pericardial layers best appreciated on ventricular systole. Patients with critical fluid accumulation (early pericardial tamponade) will have a hyperdynamic heart that demonstrates diastolic collapse of the right ventricle or atrium. (Heller M, Jehle D, [2002]. Ultrasound in Emergency Medicine [2nd Ed.] Center Page, Inc., p. 128.) Large effusions are defined as more than 1 cm wide on echocardiogram surrounding the heart.

There are currently no guidelines from the American Heart Association or the American College of Cardiology on diagnosing and managing pericardial diseases, but the European Society of Cardiology recently published useful guidelines. (Circulation 2006;113[12]:1622.) Several factors must be taken into consideration when treating a pericardial effusion, including the underlying etiology, hemodynamic significance of the effusion, and the presence of tamponade.

Symptomatic patients warrant hospital admission. Medical management is focused on alleviating the underlying etiology. Most cases of acute and viral pericarditis are self-limited and respond to medical management with nonsteroidal anti-inflammatory medications. Colchicine and steroids also may have a role, but more studies are needed. Steroids also may play an important role in autoimmune-mediated effusions. Antibiotics, antifungals, and antituberculin medications should be given to any patient at risk for a bacterial, fungal, or mycobaterial infection. Hemodynamically unstable patients may require volume resuscitation, pericardial fluid drainage, vasopressor agents, and pulmonary artery catheter placement to help guide management after emergent pericardiocentesis is performed. Patients with significant symptoms or hemodynamic instability require emergent pericardiocentesis and admission to the critical care unit with a cardiology and cardiothorasic surgery consult.

Surgical drainage and diagnostic procedures may be necessary, including pericardial window (subxyphoid pericardiostomy), thoracotomy, and video-assisted thoracic surgery. Other procedures for managing pericardial effusions include percutaneous balloon pericardiotomy, pericardial sclerosis, and external beam radiation.

This patient acutely decompensated in the intensive care unit just prior to a planned pericardial window procedure and required an emergent pericardiocentesis. This maneuver drained one liter of bloody fluid from the pericardial sac. The patient then had another liter drained by cardiothoracic surgery via a pericardial window. The fluid was found to be a malignant effusion from a lung cancer primary.

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