eMedicine Specialties > Cardiology > Pericardial Disease

Pericardial Effusion

Author: William J Strimel, DO, Fellow, Cardiovascular Disease, Scott and White Memorial Hospital
Coauthor(s): Ramin Assadi, MD, Fellow, Department of Cardiology, Loma Linda University; Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago; Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Contributor Information and Disclosures

Updated: Dec 8, 2009

Introduction

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.

Image is from a patient with malignant pericardia...

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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Image is from a patient with malignant pericardia...

Image is from a patient with malignant pericardial effusion. Note the "water-bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest film.


Pathophysiology

Embryology

In the human embryo, the pericardial cavity develops from the intraembryonic celom during the fourth week. The pericardial cavity initially communicates with the pleural and peritoneal cavities, but during normal development these are separated by the eighth week. Both the visceral and parietal pericardium are derived from the mesoderm, albeit from different parts of the embryo. The visceral pericardium develops from splanchnic mesoderm, as cells originating from the sinus venous spread out over the myocardium. The parietal pericardium derives from lateral mesoderm that covers and accompanies the developing pleuropericardial membrane, which will eventually separate the pleural and pericardial cavities. In healthy subjects, the pericardium covers the heart and great vessels, with the exception of only partially covering the left atrium.

Congenital absence of the pericardium can occur, and can be either partial or complete. It is often clinically silent, but can potentially lead to excessive cardiac motion (in the case of complete absence) causing vague chest pain or dyspnea, or, in case of partial absence with significant defects, strangulation of heart muscle and possible death.1

Physiology

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 fluid owing to its low molecular weight.

The pericardium and pericardial fluid provide important contributions to cardiac function.

  • The parietal pericardium contributes to resting diastolic pressure, and is responsible for most of this pressure in the right atrium and ventricle.
  • Through their ability to evenly distribute force across the heart, the pericardial structures assist in ensuring uniform contraction of the myocardium.
  • The normal pericardium can stretch to accommodate a small amount of fluid without significant change in intrapericardial pressure. However, once this pericardial reserve volume is surpassed, the pressure-volume curve becomes steep. With slow increases in volume, pericardial compliance can increase to lessen the increase in intrapericardial pressure.

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 L without symptoms.

Understanding the properties of the pericardium can help predict changes within the heart under physiologic stress:

  • During hypervolemic states, the pericardium limits acute cardiac cavitary dilatation.
  • By distributing forces across the heart, the pericardium plays a significant role in the physiologic concept of ventricular interdependence, whereby changes in pressure, volume, and function in one ventricle influence the function of the other.
  • The pericardium plays a pivotal role in cardiac changes during inspiration. As the right atrium and ventricle fill during normal inspiration, the pericardium, by limiting the ability of these chambers to dilate, contributes to the bowing of the atrial and ventricular septums to the left. This reduces LV filling volumes, which lead to the drop in cardiac output. As intrapericardial pressures rise, this effect becomes pronounced, eventually leading to the finding of pulsus paradoxus (discussed below), heralding the development of pericardial tamponade.

The cause of abnormal fluid production depends on the underlying etiology, but it is usually 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.

Frequency

United States

  • Few large studies have characterized the epidemiology of pericardial effusion; however, the available data consistently shows that they are more prevalent than clinically evident.
  • A higher incidence of pericardial effusion is associated with certain diseases.
  • Small pericardial effusions are often asymptomatic, and pericardial effusion has been found in 3.4% of subjects in general autopsy studies.
  • A wide variety of malignant neoplasms and hematologic malignancies can lead to pericardial effusion. Data on the prevalence varies, with some studies showing the presence of pericardial effusion as high as 21% in such patients. A large study by Bussani et al showed cardiac metastases (9.1%) and pericardial metastases (6.3%) in cases of death from all causes in individuals with an underlying carcinoma at autopsy.2 Malignancies with the highest prevalence of pericardial effusion include lung (37% of malignant effusions), breast (22%), and leukemia/lymphoma (17%).
  • Patients with HIV, with or without AIDS, are also found to have increased prevalence of pericardial effusion.3 Studies have shown the prevalence of pericardial effusion in these patients to range from 5-43%, depending on the inclusion criteria, with 13% having moderate-to-severe effusion. The incidence of pericardial effusion in patients infected with HIV has been estimated at 11%; however, whether highly active anti-retroviral therapy (HAART) has influenced this number is unknown.

Mortality/Morbidity

The mortality and morbidity of pericardial effusion is 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 HIV3

Clinical

History

A patient with pericardial effusion may report the following symptoms:

  • 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

Upon examination, a patient with pericardial effusion may have the following signs:

  • 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 H2 O 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 effusions4 )
    • 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

The following are causes of pericardial effusion.

  • Idiopathic: In most cases, the underlying cause is not identified.
  • Infectious
    • HIV infection can lead to pericardial effusion through several mechanisms, including the following:
      • Secondary bacterial infection
      • Opportunistic infection
      • Malignancy (Kaposi sarcoma, lymphoma)
      • "Capillary leak" syndrome, which is associated with effusions in other body cavities
    • Viral: The most common cause of infectious pericarditis and myocarditis is viral. Common etiologic organisms include coxsackievirus A and B, and hepatitis viruses.
    • Pyogenic (pneumococci, streptococci, staphylococci, Neisseria, Legionella species)
    • Tuberculous
    • Fungal (histoplasmosis, coccidioidomycosis, Candida)
    • Other infections (syphilitic, protozoal, parasitic)
  •  Neoplasia
    • Neoplastic disease can involve the pericardium through the following mechanisms:
      • Direct extension from mediastinal structures or the cardiac chamber
      • Retrograde extension from the lymphatic system
      • Hematologic seeding
      • As mentioned previously, the most common cases of malignant effusion are lung, breast, lymphoma, and leukemia. However, patients with malignant melanoma or mesothelioma have a high prevalence of associated pericardial effusions.
  • Postoperative/postprocedural
    • Pericardial effusions are common after cardiac surgery. In 122 consecutive patients studied serially before and after cardiac surgery, effusions were present in 103 patients; most appeared by postoperative day 2, reached their maximum size by postoperative day 10, and usually resolved without sequelae within the first postoperative month. In a retrospective survey of more than 4,500 postoperative patients, only 48 were found to have moderate or large effusions by echocardiography; of those, 36 met diagnostic criteria for tamponade.5
    • Use of preoperative anticoagulants, valve surgery, and female sex were all associated with a higher prevalence of tamponade. Symptoms and physical findings of significant postoperative pericardial effusions are frequently nonspecific, and echocardiographic detection and echo-guided pericardiocentesis, when necessary, are safe and effective; prolonged catheter drainage reduces the recurrence rate.6
    • Pericardial effusions in cardiac transplant patients are associated with an increased prevalence of acute rejection.7
  • Other less common causes include the following:

More on Pericardial Effusion

Overview: Pericardial Effusion
Differential Diagnoses & Workup: Pericardial Effusion
Treatment & Medication: Pericardial Effusion
Follow-up: Pericardial Effusion
Multimedia: Pericardial Effusion
References
Further Reading
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Further Reading

Clinical guidelines
ACR Appropriateness Criteria® acute respiratory illness in HIV-positive patient. American College of Radiology - Medical Specialty Society. 1995 (revised 2008). 6 pages. NGC:007013

Diagnosis and treatment of chest pain and acute coronary syndrome (ACS). Institute for Clinical Systems Improvement - Private Nonprofit Organization. 2004 Nov (revised 2008 Oct). 69 pages. NGC:006889

Guidelines on the diagnosis and management of pericardial diseases. The task force on the diagnosis and management of pericardial diseases of the European Society of Cardiology. European Society of Cardiology - Medical Specialty Society. 2004 Jan. 28 pages. NGC:003524

Clinical trials
Comparison the level of CTGF Protein and Related Cytokine in Pleural Effusion

Evaluation of Different Strategies of Pericardial Drainage After Aortic Valvular Surgery (Blake)

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Keywords

pericardial effusion, pleural effusion, pericardial sac, pericarditis, pericardial tamponade, cardiac tamponade, pleural effusions, pericardiocentesis, pericardial window, pericardioscopy, malignant effusion, idiopathic effusions, pulsus paradoxus, pericardial friction rub, hepatojugular reflux, Ewart sign, hydropericardium, bacterial pericardial effusion, viral pericardial effusion, tuberculous pericardial effusion, postpericardiotomy syndrome

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Contributor Information and Disclosures

Author

William J Strimel, DO, Fellow, Cardiovascular Disease, Scott and White Memorial Hospital
William J Strimel, DO is a member of the following medical societies: American College of Cardiology, American College of Physicians, and Society of Hospital Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Ramin Assadi, MD, Fellow, Department of Cardiology, Loma Linda University
Ramin Assadi, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago
Ali A Sovari, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Advanced Cardiovascular Imaging, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ronald J Oudiz, MD, FACP, FACC, Associate Professor of Medicine, Division of Cardiology, The David Geffen School of Medicine at UCLA; Director, Liu Center for Pulmonary Hypertension, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx  Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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