Pericardial effusions can occur because of a variety of causes, including excess production from an inflammatory state, damage to the cardiac chambers resulting in bleeding, decreased reabsorption because of increased systemic venous pressures in conditions such as decompensated heart failure, decreased lymphatic drainage from tumors or cancers, and lastly because of surgical manipulation of the area such as post-heart transplant.5
Most patients with pericardial effusions are asymptomatic, being discovered either on routine chest x-ray showing a globular shape to the heart or on transthoracic echocardiogram done for unrelated reasons.5
Pericardial effusions can be classified according to onset, location, hemodynamic effects, size, and composition (Table 15.1
Onset is defined as acute, subacute, or chronic. Location is circumferential, posterior, or loculated. Size is defined by echocardiographic measurement: small (<10 mm), medium (10-20 mm), and large (>20 mm) based on linear measurements of the largest echo-free space between the two layers of the pericardium at end diastole, and composition is transudative, exudative, chylous, pyopericardium, or hemopericardium.7
FIGURE 15.2 Pressure-volume curves (normal canine heart) of a pericardium after 4 weeks of chronic dilation because of volume. ( Reprinted from LeWinter MM, Kabbani S. Pericardial diseases. In: Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald’s Heart Disease: A textbook of cardiovascular medicine. 7th ed. Philadelphia, PA: Elsevier Saunders; 2005:1757-1780. Copyright © 2005 Elsevier. With permission.)
The etiology of pericardial effusions in developed countries is most often idiopathic (up to 50%) and in developing countries is tuberculosis, which has a mortality rate up to 40% in 6 months if untreated (Table 15.2
extracardiac screening should be performed, the pericardial effusion should be drained and analyzed, and a pericardial biopsy for culture and polymerase chain reaction (PCR
) should be pursued.7
Other causes include cancer (10%-25%), infections (15%-30%), iatrogenic (15%-20%), and rheumatologic (5%-15%).
TABLE 15.1 Classification of Pericardial Effusion
Acute (<1 week)
Subacute (1 week to 3 months)
Chronic (>3 months)
Size (echo-free space on echocardiography)
Mild <10 mm
Moderate 10-20 mm
Large >20 mm
TABLE 15.2 Causes of Pericardial Effusion
Viral: Enterococcus, adenovirus, herpesviruses, parvovirus B19, human immunodeficiency virus, hepatitis C, coronavirus
Bacterial: Mycobacterium (tuberculosis, avium-intracellulare), mycoplasma, Neisseria
Fungal: Histoplasma, Candida
Protozoan: Toxoplasma species
Autoimmune: Systemic lupus erythematosus, rheumatoid arthritis, scleroderma, eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome), Dressler syndrome (postmyocardial infarction)
Cardiac injury: Postmyocardial infarction, post-pericardiotomy, post-percutaneous interventions, postcardiac surgery, postablation
Neoplastic: Primary tumors (mesothelioma, sarcoma), secondary (lung, breast, lymphoma, ovarian)
Traumatic: Iatrogenic, blunt chest wall trauma
Reduced lymphatic drainage: Congestive heart failure, cirrhosis, thoracic duct occlusion
Pericardial effusions because of infections are usually exudative and, in some cases, present as pyopericardium. If infection is suspected, the pericardial effusion should be drained and sent for culture. In certain high-risk individuals, human immunodeficiency virus (HIV
) and hepatitis C screening should also be pursued.7
Systemic diseases and metabolic changes can also lead to pericardial effusions. Uremia can cause an inflammatory effusion with fibrinous material in the pericardial sac. If uremic effusion results in pericarditis, the classic uremic pericardial rub may be audible. Primary treatment for this is hemodialysis.
Other systemic conditions such as hypothyroidism, severe malnutrition, and rheumatologic diseases can also lead to pericardial effusions. Primary treatment focuses on addressing the underlying condition.1
Hemopericardium can result from injury to cardiac structures or the great vessels from either blunt force/trauma or from systemic causes. Type A aortic dissection extending to the aortic root is one example.
Lastly, new-onset symptomatic large pericardial effusions can in some cases be the first manifestation of an underlying malignancy. Malignant effusions are usually transudative and hemorrhagic and more commonly associated with extracardiac cancers (lung, breast, lymphoma) as opposed to primary cardiac tumors. Patients with chest radiation and bone marrow transplant can also have pericardial effusions.1
Chylous effusions result from obstruction of pericardial lymphatic drainage. Hence, they may occur after cardiothoracic surgery or in association with congenital lymphangiomatosis. Other causes include chest trauma, mediastinal radiation, malignant neoplasm of the mediastinum, and thrombosis of the subclavian vein or superior vena cava.
Clinical features of a pericardial effusion vary based on the acuity and rapidity of fluid accumulation. With slow accumulation, the patient may have no symptoms. Classic symptoms of rapid accumulation or large effusions include dyspnea on exertion, chest fullness or tightness, and orthopnea. Additional symptoms include nausea, hoarseness, dysphagia from compression of surrounding structures, fatigue, palpitations, and fever. On physical examination, patients may be without findings unless there is pericarditis or hemodynamic compromise from tamponade.8
When a pericardial effusion is suspected, a transthoracic echocardiogram should be performed. An echocardiogram provides semiquantitative information regarding the hemodynamic effects of the effusion, size, and location. Generally, for uncomplicated effusions, echocardiogram is sufficient for diagnosis, and rarely other imaging modalities such as cardiac computed tomography (CT) or magnetic resonance imaging (MRI
) are needed. Gated CT can be useful for delineating the effusion for surgical planning and estimating the composition based on Hounsfield units. Cardiac MRI
like echocardiography has the ability to provide both hemodynamic and anatomic assessment of the fluid. However, unlike echocardiography it can also give insight into pericardial thickening and inflammation. Therefore, MRI
can be useful in complicated cases or cases with inconclusive evidence via echocardiography.5
Management of pericardial effusion without hemodynamic compromise usually depends on the underlying etiology. Most cases (up to 60%) of pericardial effusion are associated with a known disease and the treatment is aimed at the underlying disease instead of the effusion itself. In idiopathic cases where there is concern for pericarditis, the patient should be treated as such with anti-inflammatory agents (see Acute Pericarditis, Treatment). In cases where there is no evidence of inflammation, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), or colchicine has not shown to be effective.
Pericardial effusions contributing to hemodynamic compromise (ie, cardiac tamponade, see below) should undergo urgent drainage for therapeutic (and possibly diagnostic) reasons. However, hemodynamically stable patients with a pericardial effusion do not require routine drainage or immediate drainage. Diagnostic sampling may be indicated if there is no clear etiology or when the results may alter subsequent management. The choice between percutaneous pericardiocentesis and surgical drainage depends on individual experience and specific clinical indications. Pericardiocentesis is the most common method and can be performed with echocardiographic or fluoroscopic guidance. Surgical drainage may be preferred for recurrent or loculated effusions or in cases where pericardial biopsy is needed for diagnosis.
Following pericardiocentesis, pericardial catheter is typically left in place for 24 to 48 hours or until the volume of drainage is less than 25 mL/day. Careful follow-up over days to weeks is important following pericardiocentesis to monitor for recurrence. For patients in whom pericardial fluid reaccumulates despite repeated pericardiocentesis, pericardiectomy can be considered.
Cardiac tamponade is a life-threatening condition occurring when a pericardial effusion causes hemodynamic changes resulting in cardiac collapse. It is not necessarily dependent on the size of an effusion, as the rapidity of fluid accumulation also plays a role. If an effusion accumulates acutely, it can result in tamponade with only 200 cc of fluid. Conversely, a large effusion (>2 L) may result in no or minimal hemodynamic changes if it accumulates slowly, thereby allowing time for the pericardial sac to enlarge.
Under physiologic conditions, ventricular filling occurs with little interventricular dependence because of low pericardial pressures. Inspiration decreases pericardial pressure (because of reduced intrathoracic pressure) and increases system venous return to the right atrium (Figure 15.3
). However, the decrease in intrathoracic pressure also causes decreased pulmonary venous pressure, resulting in a slight decrease in the
left ventricular (LV) preload and filling pressures. This in turn causes a slight decrease in LV stroke volume and systolic blood pressure (<10 mm Hg). In tamponade there is a substantial increase in pericardial pressure, which is directly transmitted to the cardiac chambers resulting in equalization of right ventricular (RV) and LV diastolic pressures. Therefore, during inspiration, the normal physiologic changes (such as a decrease in systolic blood pressure) are magnified resulting in substantial decreases in LV stroke volume. Furthermore, as the RV volume increases in inspiration, the interventricular septum bulges toward the left ventricle. This phenomenon is exaggerated in tamponade, further reducing LV stroke volume.7
Respiratory variation in left ventricular filling. Effective left ventricular filling pressure (eLVFP) in normal patients at baseline (A
) and with inspiration (B
) and with cardiac tamponade at baseline (C
) and with inspiration (D
). The eLVFP is the difference between the pulmonary capillary wedge pressure (PCWP
) or left atrial pressure (LAP
) and the pericardial pressure (PP). In normal patients, the PP is low and equal to the intrathoracic pressure (IT). With inspiration, the PCWP
decreases and the PP becomes negative, resulting in a net increase in the eLVFP (B
). In patients with cardiac tamponade, both the PCWP
are elevated because of the high PP (orange arrows), resulting in a lower eLVFP. With inspiration, there is increased venous return to the right side (blue arrow) and a drop in PCWP
(which lies external to the pericardium) relative to the PP, thus decreasing the eLVFP (D). The LV is consequently restrained both by pressure externally from the pericardium (orange arrows) and internally from interventricular interaction (green arrows). (Adapted from Vakamudi S, Ho N, Cremer PC. Pericardial effusions: causes, diagnosis, and management. Prog Cardiovasc Dis
. 2017;59(4):380-388. Copyright © 2017 Elsevier. With permission.)
Clinical features of a patient in tamponade include tachycardia, hypotension, muffled heart sounds, pulsus paradoxus, and increased jugular venous pressure. Electrocardiographic (ECG
) signs of tamponade can include decreased QRS voltage with electrical alternans. These clinical features correlate with the hemodynamic changes. For example, the pulsus paradoxus results from the exaggerated decrease (>10 mmHg) of systolic blood pressure during inspiration, with the magnitude of the decrease correlating with the intrapericardial pressure.5
Echocardiography is the most useful diagnostic tool in a patient with suspicion for clinical tamponade. Echocardiogram can identify the size of the effusion, location, and assess for
hemodynamic effects. Echocardiographic features of tamponade include: swinging or rocking of the heart within the pericardium, right atrial late diastolic collapse, RV early diastolic collapse, exaggerated respiratory variation with tricuspid and mitral inflow on Doppler, and abnormal ventricular septal motion.5
The hemodynamic effects of tamponade are reversed by decreasing the pericardial pressure by draining the fluid via pericardiocentesis. Elective pericardiocentesis can be done with echocardiographic or fluoroscopic guidance. In an emergency, pericardiocentesis can be accomplished via a subxiphoid approach without imaging guidance. Pericardial fluid can also be drained surgically via a pericardial window or pericardiectomy. Surgical drainage is usually reserved for effusions that are more likely to reaccumulate, such as malignant effusions or in cases with localized effusions that are difficult to drain percutaneously. Following drainage of the effusion in tamponade, patients should have continuous telemetry monitoring and frequent vital sign measures for at least 48 hours. Echocardiogram should be done prior to hospital discharge to assess for any reaccumulation of fluid. Furthermore, follow-up echocardiograms should be considered within 1 to 2 weeks following discharge and again at 6 to 12 months to evaluate for recurrence or diagnose early constriction.