Pericardial effusion is present when the fluid in the pericardial space exceeds its physiologic amount (≤50 mL). In the clinical setting, pericardial effusion is relatively common. It may be detected incidentally on a cardiac or chest imaging study, or manifest on the background of a cardiac or systemic disease.
The significance of effusions lies in their relationship to an underlying disease state and in their potential to affect a patient's hemodynamics.
Data from the Framingham cohort suggest that pericardial effusion may be present in up to 6.5% of the general adult population. Prevalence increased with age, from <1% in patients ages 20 to 30 years to more than 15% in patients ages 80 years and over. Most people in the study had small effusions and no recognizable cardiac disease.
In the clinical setting, the prevalence of pericardial effusion depends on the patient population studied. Over a 6-year period, the mean annual prevalence and incidence of pericardial effusion in an echocardiography laboratory of a large Italian hospital was 3% and 9%, respectively. In high-risk emergency department patients, the prevalence of pericardial effusion has been reported in the range of 13% to 20%.
Pericardial anatomy and physiology
The normal pericardium consists of both fibrous and serous components. The fibrous layer forms a sac that contains the heart and the roots of the great vessels. The serous part is further divided into a layer that is adherent to the heart and epicardial fat (epicardium or visceral pericardium) and a layer that lines the internal surface of the fibrous layer (parietal pericardium). The pericardial space enclosed between the visceral and the parietal pericardium normally contains up to 50 mL of serous fluid. A pericardial effusion is present when accumulated fluid in the pericardial space exceeds this physiologic amount.
The pericardium serves as a protective barrier, promotes efficient cardiac function, and prohibits excessive displacement of the heart.
Under normal conditions, a pericardial reserve volume exists to accommodate physiologic changes in ventricular filling conditions. However, if this reserve volume is exceeded, pericardial pressure increases rapidly and significantly limits cardiac filling. The relatively inelastic pericardium is able to stretch under conditions of chronic stress such as left ventricular dilation or a slowly accumulating pericardial effusion. However, once the pericardial pressure-volume relationship reaches its noncompliant stage, expansion is limited and small increases in volume produce a dramatic increase in pericardial pressure, severely impairing ventricular filling.
Classification of pericardial effusion
Pericardial effusion can be classified by:
Onset (acute or subacute vs. chronic [when lasting >3 months])
Distribution (circumferential or loculated)
Hemodynamic impact (cardiac tamponade or no cardiac tamponade)
Composition (serous fluid, blood, rarely air, or gas from bacterial infections)
Size based on a simple semiquantitative echocardiographic assessment.
Trivial (seen only in systole)
Small (<10 mm), which corresponds to 50-100 mL pericardial fluid
Moderate (10-20 mm), corresponding to 100-500 mL pericardial fluid
Large (>20 mm), corresponding to >500 mL pericardial fluid
Very large (>25 mm); usually indicates >700 mL pericardial fluid.
The development of a pericardial effusion often has important implications for the diagnosis and/or prognosis of the underlying disease.
- Bacterial pericarditis
- Tuberculous pericarditis
- Fungal pericarditis
- Chagas disease
- Systemic lupus erythematosus
- Post-myocardial infarction syndrome (Dressler phenomenon)
- Cardiac amyloidosis
- Ovarian hyperstimulation syndrome
- Aortic dissection
- Radiation exposure
Edgar Argulian, MD, MPH
Department of Cardiology
Mount Sinai St Luke's Hospital
EA is an author of one of the references cited in this topic. EA declares that he has no competing interests.
Birgit Vogel, MD
Cardiovascular Imaging Fellow
Mount Sinai St Luke's Hospital
BV declares that she has no competing interests.
Dr Edgar Argulian and Dr Birgit Vogel would like to gratefully acknowledge Dr Rajdeep Khattar, Dr David Liff, and Dr Vasilis Babaliaros, the previous contributors to this topic, and Dr Oliver Ziff for his assistance with this topic.
RK, DL, VB, and OZ declare that they have no competing interests.
Stephen Archer, MD
Professor of Medicine
Section of Cardiology
Department of Medicine
University of Chicago
Division of Biological Science
SA declares that he has no competing interests.
Shrilla Banerjee, MBChB, MD, MRCP
East Surrey Hospital
Surrey and Sussex NHS Healthcare Trust
University College London Hospitals NHS Trust
SB declares that she has no competing interests.
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