AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Pericardial effusion defines the presence of an abnormal amount and/or character of fluid in the pericardial space. It can be caused by a variety of local and systemic disorders, or it may be idiopathic. Pericardial effusions can be acute or chronic, and the time course of development has a great impact on the patient's symptoms. Treatment varies, and is directed at both removal of the pericardial fluid and alleviation of the underlying cause, which usually is determined by a combination of fluid analysis and correlation with comorbid illnesses.

Pathophysiology

The pericardial space normally contains 15-50 mL of fluid, which serves as lubrication for the visceral and parietal layers of the pericardium. This fluid is thought to originate from the visceral pericardium and is essentially an ultrafiltrate of plasma. Total protein levels are generally low; however, the concentration of albumin is increased in pericardial fluids owing to its low molecular weight.

The cause of abnormal fluid production depends on the underlying etiology, but usually it is secondary to injury or insult to the pericardium (ie, pericarditis). Transudative fluids result from obstruction of fluid drainage, which occurs through lymphatic channels. Exudative fluids occur secondary to inflammatory, infectious, malignant, or autoimmune processes within the pericardium.

Clinical manifestations of pericardial effusion are highly dependent upon the rate of accumulation of fluid in the pericardial sac. Rapid accumulation of pericardial fluid may cause elevated intrapericardial pressures with as little as 80 mL of fluid, while slowly progressing effusions can grow to 2 liters without symptoms.

Frequency

United States

Few large studies have characterized the epidemiology of pericardial effusion. Pericardial effusion has been found in 3.4% of subjects in general autopsy studies. Small pericardial effusions often are asymptomatic.

A higher incidence of pericardial effusion is associated with certain diseases. Twenty-one percent of cancer patients have metastases to the pericardium. The most common are lung (37% of malignant effusions), breast (22%), and leukemia/lymphoma (17%). Patients with HIV, with or without AIDS, are found to have increased prevalence, with 41-87% having asymptomatic effusion and 13% having moderate-to-severe effusion.

Mortality/Morbidity

Dependent upon etiology and comorbid conditions

• Idiopathic effusions are well tolerated in most patients. As many as 50% of patients with large, chronic effusions were asymptomatic during long-term follow-up.
• Pericardial effusion is the primary or contributory cause of death in 86% of cancer patients with symptomatic effusions.
• Survival rate for patients with HIV and symptomatic pericardial effusion is 36% at 6 months, 19% at 1 year.

Race

• No consistent difference among races is reported in the literature.
• AIDS patients with pericardial effusion are more likely to be white.

Sex

• No sexual predilection exists.

Age

• Observed in all age groups
• Mean occurrence in fourth or fifth decades; earlier in patients with HIV

CLINICAL

Section 3 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

• Cardiovascular
• • Chest pain, pressure, discomfort: Characteristically, pericardial pain may be relieved by sitting up and leaning forward and is intensified by lying supine.
  • Light-headedness, syncope
  • Palpitations
• Respiratory - Cough, dyspnea, hoarseness
• Gastrointestinal - Hiccoughs
• Neurologic - Anxiety, confusion

Physical

• Cardiovascular
• • Classic Beck triad of pericardial tamponade (hypotension, muffled heart sounds, jugular venous distension)
  • Pulsus paradoxus: Exaggeration of physiologic respiratory variation in systemic blood pressure, defined as a decrease in systolic blood pressure of more than 10 mm Hg with inspiration, signaling falling cardiac output during inspiration.
  • Pericardial friction rub: The most important physical sign of acute pericarditis may have up to 3 components per cardiac cycle and is high-pitched, scratching, and grating. It can sometimes be elicited only when firm pressure with the diaphragm of the stethoscope is applied to the chest wall at the left lower sternal border. The pericardial friction rub is heard most frequently during expiration with the patient upright and leaning forward.
  • Tachycardia
  • Hepatojugular reflux: This can be observed by applying pressure to the periumbilical region. A rise in the jugular venous pressure (JVP) of greater than 3 cm H₂O for more than 30 seconds suggests elevated central venous pressure. Transient elevation in JVP may be normal.
• Respiratory
• • Tachypnea
  • Decreased breath sounds (secondary to pleural effusions)
  • Ewart sign - Dullness to percussion beneath the angle of left scapula from compression of the left lung by pericardial fluid
• Gastrointestinal - Hepatosplenomegaly
• Extremities
• • Weakened peripheral pulses
  • Edema
• Cyanosis

Causes

• Infectious
• • Viral (coxsackievirus A and B, hepatitis, HIV)
  • Pyogenic (pneumococci, streptococci, staphylococci, Neisseria, Legionella species)
  • Tuberculous
  • Fungal (histoplasmosis, coccidioidomycosis, Candida)
  • Other infections (syphilitic, protozoal, parasitic)
• Noninfectious
• • Acute idiopathic
  • Uremia
  • Neoplasia
    • Primary tumors (benign or malignant, mesothelioma)
    • Tumors metastatic to pericardium (lung and breast cancer, lymphoma, leukemia)
  • Myxedema
  • Acute myocardial infarction
  • Postirradiation
  • Aortic dissection (with leakage into pericardial sac)
  • Trauma
  • Cholesterol
  • Chylopericardium
  • Familial Mediterranean fever
  • Whipple disease
  • Sarcoidosis
• Hypersensitivity or autoimmunity related
• • Rheumatic fever
  • Collagen vascular disease (systemic lupus erythematosus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, acute rheumatic fever, Wegener granulomatosis)
  • Drug-induced (eg, procainamide, hydralazine, isoniazid, minoxidil, phenytoin, anticoagulants, methysergide)
  • Postcardiac injury

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

WORKUP

Section 5 of 12  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

• Electrolytes - Metabolic abnormalities (eg, renal failure)
• CBC count with differential - Leukocytosis for evidence of infection, as well as cytopenias, as signs of underlying chronic disease (eg, cancer, HIV)
• Cardiac enzymes: Troponin level is frequently minimally elevated in acute pericarditis, usually in the absence of an elevated total creatine kinase level. Presumably, this is due to some involvement of the epicardium by the inflammatory process. Although the elevated troponin may lead to the misdiagnosis of acute pericarditis as a myocardial infarction, most patients with an elevated troponin and acute pericarditis have normal coronary angiograms. An elevated troponin level in acute pericarditis typically returns to normal within 1-2 weeks and is not associated with a worse prognosis.
• Thyroid-stimulating hormone - Thyroid-stimulating hormone screen for hypothyroidism
• Rickettsial antibodies - If high index of suspicion of tick-borne disease
• Rheumatoid factor, immunoglobulin complexes, antinuclear antibody test (ANA), and complement levels (which would be diminished) - In suspected rheumatologic causes
• Pericardial fluid analysis - Routine tests
• • Lactic (acid) dehydrogenase (LDH), total protein - The Light criteria (for exudative pleural effusion) found to be as reliable in distinguishing between exudative and transudative effusions
    • Total protein fluid-to-serum ratio >0.5
    • LDH fluid-to-serum ratio >0.6
    • LDH fluid level exceeds two thirds of upper-limit of normal serum level
  • Other indicators suggestive of exudate - Specific gravity >1.015, total protein >3.0 mg/dL, LDH >300 U/dL, glucose fluid-to-serum ratio <1
  • Cell count - Elevated leukocytes (ie, >10,000) with neutrophil predominance suggests bacterial or rheumatic cause, although unreliable
  • Gram stain - Specific but insensitive indicator of bacterial infection
  • Cultures - Signals and identifies infectious etiology
  • Fluid hematocrit for bloody aspirates - Hemorrhagic fluid hematocrits usually significantly less than simultaneous peripheral blood hematocrits
• Pericardial fluid - Special tests
• • Viral cultures
  • Adenosine deaminase; polymerase chain reaction (PCR); culture for tuberculosis; smear for acid-fast bacilli in suspected tuberculosis infection, especially in patients with HIV
  • A definite diagnosis of tuberculous pericarditis is based on the demonstration of tubercle bacilli in pericardial fluid or on a histological section of the pericardium. Probable tuberculous pericarditis is based on the proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated adenosine deaminase levels, and/or appropriate response to a trial of antituberculosis chemotherapy.

Imaging Studies

• Chest radiography
• • Findings include enlarged cardiac silhouette (so-called water-bottle heart), pericardial fat stripe (see Image 1).
  • A third of patients have a coexisting pleural effusion.
  • Radiography is unreliable in establishing or refuting diagnosis of pericardial effusion.
• Echocardiogram
• • This is the criterion standard for noninvasive diagnosis (see Image 2).
  • Pericardial effusion appears as an "echo-free" space between the visceral and parietal pericardium (see Image 3). Early effusions tend to accumulate posteriorly owing to expandable posterior/lateral pericardium. Large effusions are characterized by excessive motion within the pericardial sac. Severe cases may be accompanied by diastolic collapse of the right atrium and right ventricle (and in hypovolemic patients the left atrium and left ventricle), signaling the onset of pericardial tamponade (see Cardiac Tamponade).
  • Large pericardial effusions are defined as greater than 1 cm thick on echocardiography, completely surrounding the heart. Small effusions are less than 1 cm and often localized, usually posteriorly.
  • False-positive echocardiograms can occur in pleural effusions, pericardial thickening, increased pericardial fat (especially the anterior epicardial fat pad), atelectasis, and mediastinal lesions.
  • In patients with pericardial effusion, imaging from low to midposterior thorax can provide additional diagnostic echocardiographic images and should be used in patients in whom conventional images are technically difficult or require additional information.
• Transesophageal echocardiography: Transesophageal echocardiography (TEE) is useful in characterizing loculated effusions.
• CT scan
• • Potentially can determine composition of fluid and may detect as little as 50 mL of fluid
  • Fewer false-positive results than with echocardiography
  • Problem: Patients must be transported to the CT scanner, which may not be possible if the patient's condition is unstable.
• MRI
• • Can detect as little as 30 mL of pericardial fluid
  • May be able to distinguish hemorrhagic and nonhemorrhagic effusions
  • More difficult to perform than CT scan acutely, given the length of time the patient must remain in the scanner
• Both MRI and CT scan may be superior to echocardiography in detecting loculated pericardial effusions and pericardial thickening

Other Tests

• ECG
• • Early in the course of acute pericarditis, the ECG typically displays diffuse ST elevation in association with PR depression. The ST elevation is usually present in all leads except for aVR, but post–myocardial infarction pericarditis, the changes may be more localized. Classically, the ECG changes of acute pericarditis evolve through 4 progressive stages: stage I, diffuse ST-segment elevation and PR-segment depression; stage II, normalization of the ST and PR segments; stage III, widespread T-wave inversions; and stage IV, normalization of the T waves (see Image 4).
  • Patients with uremic pericarditis frequently do not have the typical ECG abnormalities.

Procedures

• Pericardiocentesis
• • This procedure is used for diagnostic as well as therapeutic purposes. Support for the use of echocardiographic guidance is increasing, unless emergent treatment is required.
  • Indications include impending hemodynamic compromise (ie, pericardial tamponade), suspected infectious etiology, and uncertain etiology.
  • Use of a needle that is at least 5 cm long, 16-gauge in diameter, and has a short bevel can minimize the risk of complications and should allow for adequate pericardial drainage. A system allowing placement of a catheter over the needle is preferred.
  • Contrast echocardiography using agitated saline is useful in cases when bloody fluid is aspirated to determine if the needle is in the ventricular cavity.
  • Attaching an ECG electrode to the pericardiocentesis needle is also useful for avoiding myocardial puncture. Electrical activity will be seen on the monitor when the needle comes into contact with atrial or ventricular myocardium. These changes may be delayed, however, and instill a false sense of security in needle placement; sense of touch and the findings on aspiration should guide the procedure, with the clinician ultimately relying on good clinical sense.
  • Complications of pericardiocentesis include ventricular rupture, dysrhythmias, pneumothorax, myocardial and/or coronary artery laceration, and infection.
  • Recurrence rates within 90 days may be as high as 90% in patients with cancer.
• Balloon pericardotomy
• • A catheter is placed in the pericardial space under fluoroscopy, which, after inflation of the balloon, creates a channel for passage of fluid into the pleural space, where reabsorption occurs more readily.
  • This may be useful for recurrent effusions.
• Pericardial sclerosis
• • Several pericardial sclerosing agents have been used with varying success rates (eg, tetracycline, doxycycline, cisplatin, 5-fluorouracil).
  • The pericardial catheter may be left in place for repeat instillation if necessary until the effusion resolves.
  • Complications include intense pain, atrial dysrhythmias, fever, and infection.
  • Success rates are reported as high as 91% at 30 days.
• Pericardioscopy
• • This procedure is not universally available.
  • It may increase diagnostic sensitivity in cases of unexplained pericardial effusions. It allows for visualization of pericardium and for pericardial biopsies.

TREATMENT

Section 6 of 12  

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Medical Care

Initially, medical care is focused on determination of the underlying etiology.

• Aspirin/nonsteroidal anti-inflammatory agents (NSAIDs)
• • Most acute idiopathic or viral pericarditis occurrences are self-limited and respond to treatment with aspirin (650 mg q6h) or another NSAID.
  • Aspirin may be the preferred nonsteroidal agent to treat pericarditis after myocardial infarction because other NSAIDs may interfere with myocardial healing.
  • Indomethacin should be avoided in patients who may have coronary artery disease.
• Colchicine: The routine use of colchicine is supported by recently reported results of the COlchicine for acute PEricarditis (COPE) trial. In this trial, 120 patients with a first episode of acute pericarditis (idiopathic, acute, postpericardiotomy syndrome, and connective tissue disease) entered a randomized, open-label trial comparing aspirin treatment alone with aspirin plus colchicine (1-2 mg for the first day followed by 0.5-1 mg/d for 3 mo). Colchicine reduced symptoms at 72 hours (11.7% vs 36.7%; P=0.03) and reduced recurrence at 18 months (10.7% vs 36.7%; P=0.004; 5 needed treatment). Colchicine was discontinued in 5 patients because of diarrhea. No other adverse events were noted. Importantly, none of the 120 patients developed cardiac tamponade or progressed to pericardial constriction.
• Steroids
  • Steroid administration early in the course of acute pericarditis appears to be associated with an increased incidence of relapse after tapering the steroids.
  • In the COPE trial, steroid use was an independent risk factor for recurrence (odds ratio=4.3). Also, an observational study strongly suggests that the use of steroids increases the probability of relapse in patients treated with colchicine.
  • Systemic steroids should be considered only in patients with recurrent pericarditis unresponsive to NSAIDs and colchicine or as needed for treatment of an underlying inflammatory disease. If steroids are to be used, an effective dose (1-1.5 mg/kg of prednisone) should be given, and it should be continued for at least 1 month before slow tapering.
  • The intrapericardial administration of steroids has been reported to be effective in acute pericarditis without producing the frequent reoccurrence of pericarditis that complicates the use of systemic steroids, but the invasive nature of this procedure limits its use.
• Hemodynamic support
• • Patients who have effusions with actual or threatened tamponade should be considered to have a true or potential emergency. Most patients require pericardiocentesis to treat or prevent tamponade. However, treatment should be carefully individualized.
  • Hemodynamic monitoring with a balloon flotation pulmonary artery catheter is useful, especially in those with threatened or mild tamponade in whom a decision is made to defer pericardiocentesis. Hemodynamic monitoring is also helpful after pericardiocentesis to assess both reaccumulation and the presence of underlying constrictive disease. However, insertion of a pulmonary artery catheter should not be allowed to delay definitive therapy in critically ill patients.
  • Intravenous fluid resuscitation may be helpful in cases of hemodynamic compromise.
  • In patients with tamponade who are critically ill, intravenous positive inotropes (dobutamine, dopamine) can be used but are of limited measures and should not be allowed to substitute for or delay pericardiocentesis.
• Antibiotics
  • In patients with purulent pericarditis, urgent pericardial drainage combined with intravenous antibacterial therapy (eg, vancomycin 1 g bid, ceftriaxone 1-2 g bid, and ciprofloxacin 400 mg/d) is mandatory. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable.
  • The initial treatment of tuberculous pericarditis should include isoniazid 300 mg/day, rifampin 600 mg/day, pyrazinamide 15-30 mg/kg/day, and ethambutol 15-25 mg/kg/day. Prednisone 1-2 mg/kg/day is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Uncertainty remains whether adjunctive corticosteroids are effective in reducing mortality or progression to constriction. Surgical resection of the pericardium remains the appropriate treatment for constrictive pericarditis. The timing of surgical intervention is controversial, but many experts recommend a trial of medical therapy for noncalcific pericardial constriction and pericardiectomy in nonresponders after 4-8 weeks of antituberculosis chemotherapy.
• Antineoplastic therapy (eg, systemic chemotherapy, radiation) in conjunction with pericardiocentesis has been shown to be effective in reducing recurrences of malignant effusions.
• Corticosteroids and NSAIDs are helpful in patients with autoimmune conditions.

Surgical Care

• Subxiphoid pericardial window with pericardiostomy
• • This procedure is associated with low morbidity, mortality, and recurrence rates.
  • It can be performed under local anesthesia.
  • It may be less effective when effusion is loculated.
  • It may replace pericardiocentesis as initial treatment for stable pericardial effusions.
  • A recent study suggests that this may be safer and more effective at reducing recurrence rates than pericardiocentesis. However, only patients who were hemodynamically unstable underwent pericardiocentesis, and no change in overall survival rate was observed.
• Thoracotomy
• • This should be reserved for patients in whom conservative approaches have failed.
  • Thoracotomy allows for creation of a pleuropericardial window, which provides greater visualization of pericardium.
  • Thoracotomy requires general anesthesia and thus has higher morbidity and mortality rates than the subxiphoid approach.
• Video-assisted thoracic surgery
• • Video-assisted thoracic surgery (VATS) enables resection of a wider area of pericardium than the subxiphoid approach without the morbidity of thoracotomy.
  • The surgeon is able to create a pleuropericardial window and address concomitant pleural pathology, which is especially common in patients with malignant effusions.
  • One disadvantage of VATS is that it requires general anesthesia with single lung ventilation, which may be difficult in otherwise seriously ill patients.
• Median sternotomy
• • This procedure is reserved for patients with constrictive pericarditis.
  • Operative mortality rate is high (5-15%).

Consultations

• A cardiologist should be involved in the care of patients with pericardial effusion.
• Cardiothoracic surgery may be required for recurrent or complicated cases (see Surgical Care).

MEDICATION

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Autoimmune pericardial effusions may respond to treatment with anti-inflammatory medications. In general, selection of an agent depends on the severity of the patient's symptoms and the tolerability and adverse effect profiles of the medications.

Drug Category: Nonsteroidal anti-inflammatory drugs

Are used mostly for patients with active, nonhemorrhagic pericarditis with or without pericardial effusion. NSAIDS have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action in pericarditis is not known, but NSAIDS may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Drug Category: Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

FOLLOW-UP

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Further Inpatient Care

• Patients who present with significant symptoms or cardiac tamponade require emergent treatment and admission to ICU.
• The pericardial catheter (if placed) should be removed within 24-48 hours to avoid infection.
• Symptomatic patients should remain hospitalized until definitive treatment is accomplished and/or symptoms have resolved.

Further Outpatient Care

• Patients should be educated on symptoms of increasing pericardial effusion and should be evaluated whenever these symptoms begin to occur.
• Indications for echocardiography after diagnosis include the following:
• • A follow-up imaging study to evaluate for recurrence/constriction: Repeat studies may be performed to answer specific clinical questions.
  • The presence of large or rapidly accumulating effusions (to detect early signs of tamponade)

Transfer

• Symptomatic patients requiring treatment (who are surgical candidates) should receive care at an institution with cardiothoracic surgery capabilities.

Complications

• Pericardial tamponade
• • Can lead to severe hemodynamic compromise and death
  • Heralded by equalization of diastolic filling pressures
  • Treat with expansion of intravascular volume (small amounts of crystalloids or colloids may lead to improvement, especially in hypovolemic patients) and urgent pericardial drainage. Avoid positive-pressure ventilation if possible, as this decreases venous return and cardiac output. Vasopressor agents are of little clinical benefit.
• Chronic pericardial effusion
• • Effusions lasting longer than 6 months
  • Usually well tolerated

Prognosis

• Most patients with acute pericarditis recover without sequelae. Predictors of a worse outcome include the following: fever greater than 38°C, symptoms developing over several weeks in association with immunosuppressed state, traumatic pericarditis, pericarditis in a patient receiving oral anticoagulants, a large pericardial effusion (>20 mm echo-free space or evidence of tamponade), or failure to respond to NSAIDs. In a recent series of 300 patients with acute pericarditis, 254 (85%) did not have any of the high-risk characteristics and had no serious complications. Of these low-risk patients, 221 (87%) were managed as outpatients and the other 13% were hospitalized when they did not respond to aspirin.
• Patients with symptomatic pericardial effusions from HIV/AIDS or cancer have high short-term mortality rates.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to consider pericardial effusion as a principal or secondary diagnosis may lead to rapid deterioration and death secondary to cardiac tamponade.
• Patients with viral cardiomyopathy, especially in the acute setting, may have a similar presentation, with an enlarged heart on chest radiographs. Echocardiography readily distinguishes the difference between enlarged cardiac chambers and a pericardial effusion.

ACKNOWLEDGMENTS

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The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Susan Noe, MD, to the development and writing of this article.

MULTIMEDIA

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• Acknowledgments
• Multimedia
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Media file 1:  Image is from a patient with malignant pericardial effusion. Note the "water-bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest film.
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Media type:  X-RAY

Media file 2:  Echocardiogram (parasternal, long axis) of a patient with a moderate pericardial effusion.
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Media type:  Image

Media file 3:  This image is from the same patient with malignant pericardial effusion shown in Images 1 and 4. The effusion is seen as an echo-free region to the right of the left ventricle (LV).
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Media type:  Image

Media file 4:  This ECG is from the same patient with malignant pericardial effusion shown in Images 1 and 3. The ECG shows diffuse low voltage, with a suggestion of electrical alternans in the precordial leads.
	View Full Size Image
Media type:  ECG

REFERENCES

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• References

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• Kasper D, Branunwald E, Fauci A, et al. Harrison's Principles of Internal Medicine. 16th ed. McGraw-Hill Professional;2005:1414-1420.
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Article Last Updated: Sep 7, 2006