Summary
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.
Epidemiology
Data from the Framingham cohort suggest that pericardial effusion may be present in up to 6.5% of the general adult population.[1] 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.[1]
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.[2] In high-risk emergency department patients, the prevalence of pericardial effusion has been reported in the range of 13% to 20%.[3] One meta-analysis reported pooled pericardial effusion prevalence of 19.5% across studies that included patients with pulmonary arterial hypertension, chronic heart failure, myocardial infarction, and malignancy.[4]
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.[5]
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.[Figure caption and citation for the preceding image starts]: Diagram showing the anatomy of the pericardium.Marchand P. Thorax. 1951;6:359-368 [Citation ends].
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.
The size of the effusion on echocardiography indicates the volume of pericardial fluid as follows:[5][6][7]
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.[5]
Differentials
Common
- Malignancy
- Viral pericarditis
- Iatrogenic
- Idiopathic
- Congestive heart failure
- Uremia
Uncommon
- Bacterial pericarditis
- Tuberculous pericarditis
- Fungal pericarditis
- Chagas disease
- Systemic lupus erythematosus
- Post-myocardial infarction syndrome (Dressler phenomenon)
- Drug-induced
- Cardiac amyloidosis
- Hypothyroidism
- Ovarian hyperstimulation syndrome
- Aortic dissection
- Trauma
- Radiation exposure
Contributors
Authors
Edgar Argulian, MD, MPH
Assistant Professor
Department of Cardiology
Mount Sinai St Luke's Hospital
New York
NY
Disclosures
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
New York
NY
Disclosures
BV declares that she has no competing interests.
Acknowledgements
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.
Disclosures
RK, DL, VB, and OZ declare that they have no competing interests.
Peer reviewers
Stephen Archer, MD
Professor of Medicine
Section of Cardiology
Department of Medicine
University of Chicago
Division of Biological Science
Chicago
IL
Disclosures
SA declares that he has no competing interests.
Shrilla Banerjee, MBChB, MD, MRCP
Consultant Cardiologist
East Surrey Hospital
Surrey and Sussex NHS Healthcare Trust
Redhill
Surrey
Heart Hospital
University College London Hospitals NHS Trust
London
UK
Disclosures
SB declares that she has no competing interests.
Use of this content is subject to our disclaimer