Pericardial effusion is a frequent finding that occurs due to primary pericardial disease or in relation to a myriad of systemic disease processes. The significance of effusions lies in their relationship to an underlying disease state and in their potential to affect a patient's haemodynamics.
Data from the Framingham cohort suggest that pericardial effusion may be present in up to 6.5% of the adult population. In the Framingham cohort, the incidence increased with age, with only 1.2% of patients <50 years of age having effusion detected on echocardiogram. Most people with effusions had no recognisable cardiac disease. Overall, the incidence of more than a small effusion is very low.
Pericardial anatomy and physiology
The normal pericardium consists of 2 layers, the visceral and parietal pericardia, separated by 15 to 35 mL of fluid. The normal pericardial fluid is an ultrafiltrate of plasma and characteristically has a low protein concentration and low specific gravity. The parietal pericardium is an inelastic fibrous structure consisting largely of collagen that reflects off the great vessels and various other thoracic structures to provide stability for the heart. It also acts as a barrier to infection.
The semi-rigid properties of the pericardium serve as a constraint on cardiac filling and promote ventricular interdependence. Under normal conditions, a pericardial reserve volume exists to accommodate physiological 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 grow under conditions of chronic stress such as left ventricular dilation or a slowly accumulating pericardial effusion, although once the pericardial pressure-volume relationship reaches its non-compliant stage, expansion is limited and small increases in volume produce a dramatic increase in pericardial pressure, severely impairing ventricular filling.
Types of pericardial effusion
The mechanism of abnormal fluid collection depends on the underlying aetiology, but is typically due to injury of the pericardium and may be classified as acute or chronic, and small or large. Chronic effusion has been defined as an effusion that persists for >3 months; and acute, as <3 months. The size of an effusion is variably defined. However, when the sum of anterior and posterior echo-free spaces exceeds 20 mm, the effusion is generally considered large.
The fluid may be serous, purulent, haemorrhagic, chylous, or serosanguineous, but the nature of the effusion adds little to the characterisation of the aetiology. Effusions are categorised as transudates or exudates. Exudative effusions may be idiopathic, iatrogenic, or due to infection, malignancy, trauma, cardiorespiratory, and autoimmune processes. Exudative effusions result from acute or chronic pericardial inflammation, with high levels of protein.
Cardiac tamponade occurs when pericardial pressure increases and limits cardiac filling. The severity of tamponade is determined by its effect on cardiac output and haemodynamics, but even when hypotension is not present, tamponade is a serious condition that may rapidly progress and requires urgent evaluation. Effusions that are small and thought to be transudative are unlikely to be clinically significant.
Chronic pericardial effusion may share similar clinical symptoms and signs with pericardial constriction. The 2 conditions may co-exist, or constriction may develop as a later consequence of the underlying aetiology of the pericardial effusion, particularly following tuberculous pericarditis or after cardiac surgery. Differentiating these 2 conditions may be difficult and requires advanced imaging techniques.
Consultant Cardiologist and Honorary Clinical Senior Lecturer
Department of Cardiology
Royal Brompton Hospital
RK declares that he has no competing interests.
Dr Rajdeep Khattar would like to gratefully acknowledge Dr David Liff and Dr Vasilis Babaliaros, the previous contributors to this monograph, and Dr Oliver Ziff for his assistance with this monograph. DL, VB, and OZ declare that they have no competing interests.
Professor of Medicine
Section of Cardiology
Department of Medicine
University of Chicago
Division of Biological Science
SA declares that he has no competing interests.
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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