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Echocardiographic evaluation of the pericardium

Echocardiographic evaluation of the pericardium
Author:
Elyse Foster, MD
Section Editor:
Warren J Manning, MD
Deputy Editor:
Susan B Yeon, MD, JD
Literature review current through: Jan 2024.
This topic last updated: Mar 15, 2023.

INTRODUCTION — Transthoracic echocardiography (TTE) is the initial method of choice for evaluating most pericardial diseases, given its ability to provide both anatomic and physiologic/hemodynamic information. When competently performed in patients with good acoustic windows, TTE accurately detects pericardial effusions and provides clinically relevant information about their size and hemodynamic importance.

This topic will discuss the TTE approach to evaluating the pericardium, along with normal pericardial anatomy, indications for performing TTE, and a brief description of some pericardial pathologic processes. Detailed discussions of pericardial pathology, along with the imaging evaluation of the pericardium in particular disease states, are presented separately. (See "Pericardial effusion: Approach to diagnosis" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic evaluation".)

NORMAL PERICARDIUM — The normal pericardium is a fibroelastic sac containing a thin layer of fluid that surrounds the heart.

Normal anatomy — The normal pericardium consists of two layers: a fibrous outer layer and a serous inner layer. The serous layer is a closed sac with the visceral component lining the epicardium and the parietal component lining the fibrous outer layer. The outer fibrous pericardium produces one of the most strongly reflective or echo-producing areas of the heart, and it normally moves anteriorly with the epicardium. The pericardium is reflected from the pulmonary veins as they enter the left atrium. The fibrous component has attachments to the sternum and to the diaphragm [1].

Normally, a small amount of fluid (less than 50 mL) is contained within the closed sac of the serous layer. Because of the pericardial reflection at the level of the pulmonary veins, pericardial fluid rarely accumulates in this area posterior to the left atrium because the potential space available decreases abruptly.

Pericardial fat is also commonly seen on two-dimensional (2D) TTE (movie 1). Accumulation is most common in the interventricular and atrioventricular grooves and on the right ventricular (RV) free wall. This normal but highly variable finding is most commonly seen anterior to the heart in the parasternal long axis view and in the subcostal views. The best clues to its identity as fat are its absence posteriorly, normal motion of the pericardium, and low intensity echoes (often seen as faint linear striations) within the pericardial space.

Normal physiology — In patients with a normal pericardium, intrathoracic pressure decreases during inspiration, leading to an increase in venous return to the right heart and transient increase in RV chamber size. Because the normal pericardium accommodates the increased venous return by stretching, this increase in venous return does not impair left ventricular (LV) filling.

Normal appearance on echocardiographic imaging — When visualized on 2D echocardiography, the layers of the pericardium appears as thin echogenic lines surrounding the myocardium. The normal thickness of the visualized pericardial layers is less than 3 mm by echocardiography [2], but it can be difficult to make accurate measurements due to suboptimal image quality and motion throughout the cardiac cycle.

In the normal healthy pericardium, there is less than 50 mL of serous fluid in the pericardial sac formed by these layers [3]. The interposition of this fluid between the pericardial layers can result in a very small physiological separation of the layers, which may be appreciated on M-mode echocardiography only during systole (image 1 and movie 2).

When inspecting the pericardium in a real-time 2D TTE examination, it is important to appreciate the motion of the heart within it. Normally, the heart and epicardial pericardium move and twist within the parietal pericardium.

In the short axis, the motion is due to the twisting of the heart during systole and untwisting during diastole.

In the apical four chamber view, the motion is due to both the torsion and the longitudinal muscle shortening.

The four chamber sub-costal view is particularly useful in detection of the motion between the pericardial layers. This normal independent motion is impaired or lost when pericardial inflammation and/or scarring results in adhesions between the visceral and parietal layers.

INDICATIONS — Various professional societies have made recommendations for the use of TTE in the evaluation of suspected pericardial disease [2,4-6].

In general, TTE should be part of the routine imaging evaluation in the following circumstances:

All patients with suspected pericardial disease, including effusion, constrictive pericarditis, or effusive-constrictive pericarditis.

All patients with suspected bleeding into the pericardial space (eg, trauma, perforation, postoperative).

Follow-up study to evaluate pericardial effusion progression, recurrence of pericardial effusion following treatment, or to diagnose early constrictive pericarditis.

Patients with pericardial friction rub developing in acute myocardial infarction (MI) accompanied by symptoms such as persistent pain, hypotension, and nausea. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Pericardial friction rub'.)

Echocardiography can be somewhat limited for diagnosing loculated effusions. Both cardiovascular magnetic resonance (CMR) and cardiac computed tomography (CT) are generally preferred to echocardiography for measuring pericardial thickness and identifying loculated effusions, with CMR providing greater discrimination between pericardium and small pericardial effusions [2]. CT is preferable for detecting pericardial calcification. CMR is the preferred method to identify pericardial inflammation/pericarditis. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'CMR and/or CT'.)

PERICARDIAL COMPRESSIVE SYNDROMES — When pericardial fluid accumulates (pericardial effusion) or when the pericardium becomes scarred and inelastic, one of three pericardial compressive syndromes may occur:

Cardiac tamponade – Cardiac tamponade, which may be acute or subacute, is characterized by the accumulation of pericardial fluid under pressure. Variants include low pressure (occult) and regional cardiac tamponade. (See "Cardiac tamponade" and 'Pericardial effusion' below.)

Constrictive pericarditis – Constrictive pericarditis is the result of scarring and consequent loss of elasticity of the pericardial sac. Pericardial constriction is typically chronic, but variants include subacute, transient, and occult constriction. (See "Constrictive pericarditis: Diagnostic evaluation" and 'Pericardial thickening and constrictive pericarditis' below.)

Effusive-constrictive pericarditis – Effusive-constrictive pericarditis is characterized by underlying constrictive physiology with a coexisting pericardial effusion, usually with cardiac tamponade. Such patients may be mistakenly thought to have only cardiac tamponade; however, persistent elevation of the right atrial and pulmonary capillary wedge pressures after drainage of the pericardial fluid points to the underlying constrictive process. (See "Constrictive pericarditis: Diagnostic evaluation" and 'Pericardial thickening and constrictive pericarditis' below.)

CONDITIONS ASSOCIATED WITH PERICARDIAL PATHOLOGY — Pericardial abnormalities can result from a number of cardiac and systemic conditions [6].

Acute pericarditis — The TTE is often normal in patients with the clinical syndrome of acute pericarditis unless it is associated with increased pericardial fluid/abnormal pericardial effusion, which is present in approximately 60 percent of patients [7]. While the finding of more than trivial pericardial effusion in a patient with known or suspected pericarditis supports the diagnosis, the absence of a pericardial effusion or other echocardiographic abnormalities does not exclude it. Large and/or hemodynamically significant pericardial effusions are rare as the initial presentation of acute pericarditis. CMR is the preferred imaging method to diagnose the pericardial inflammation seen in pericarditis. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Echocardiogram' and "Acute pericarditis: Clinical presentation and diagnosis", section on 'CMR and/or CT'.)

Pericardial effusion — TTE has an important role in diagnosing the presence of pericardial effusion, estimating the relative size of the effusion, and evaluating the hemodynamic importance of an effusion (movie 3 and movie 4 and movie 5 and movie 6). Key elements of the pericardial effusion which should be described include size (maximal thickness and if it varies by location) and location (circumferential versus loculated).

A transudative pericardial fluid appears on an echocardiogram as an echolucent (dark) space between the pericardium and the epicardium. Small collections of pericardial fluid, which can be physiologic (up to 50 mL), may be visible during ventricular systole. Effusions exceeding 50 mL are seen as an echo-free space throughout the cardiac cycle. Typically, a small (50 to 100 mL) free-flowing pericardial effusion is seen posterior to the LV; this space diminishes and finally disappears as the echo beam approaches the base of the LV and the left atrium (image 2). Accumulation of pericardial fluid above the right atrium in the apical four chamber view with the patient in the left lateral decubitus position is, perhaps, the single most sensitive and specific indication of a pericardial effusion (image 3). However, in the case of a free-flowing effusion, the site of accumulation may be positional as there is gravity dependence. As the effusion increases in size, it is typically seen anterior to the RV and best seen from the subcostal view.

The size of a pericardial effusion is graded semi-quantitatively, and when measured, it is measured in diastole.

Small effusions (50 to 100 mL) are only seen posteriorly, typically less than 10 mm in thickness, and only cause minimal separation between the epicardial (visceral) pericardium and the thicker parietal pericardial sac.

Moderate effusions (100 to 500 mL) tend to be seen along the length of the posterior wall but not anteriorly; the echo-free space is 10 to 20 mm at its greatest width.

Large effusions (>500 mL) tend to be seen circumferentially (image 4 and image 5); the echo-free space is greater than 20 mm at its greatest width.

The pericardial effusion should be described as circumferential or loculated and transudative or exudative. Exudative effusions are echo-filled. Additionally, though size is relevant (as mentioned earlier) the hemodynamic consequence of a pericardial effusion is also related to the rate of fluid accumulation. Echocardiography is also helpful to determine if the effusion can be drained percutaneously and to assist monitoring during pericardiocentesis. (See "Cardiac tamponade" and "Pericardial effusion: Approach to management", section on 'Echocardiography'.)

Loculated effusion and other postoperative sequelae — Pericardial fluid ceases to be circumferential and free flowing and becomes loculated or compartmentalized as a result of a variety of disease processes, most commonly following cardiac surgery or following pericardial hemorrhage (eg, as a complication of percutaneous coronary intervention or pacemaker lead placement). Pericardial stranding, suggestive of fibrous material within the pericardial effusion, is easily seen on echocardiographic imaging, often as a precursor to loculation of the effusion (movie 7).

A loculated, eccentric effusion or localized hematoma can produce regional cardiac tamponade in which only selected chambers are compressed. Regional cardiac tamponade is most often seen after pericardiotomy or MI. Clinical suspicion should be heightened in these settings. Establishing the diagnosis is challenging and may require additional echocardiographic views (eg, subcostal or transesophageal echocardiography) and other advanced imaging techniques (eg, CT). (See "Cardiac tamponade" and "Post-cardiac injury syndromes".)

Differentiating between pleural and pericardial effusions — Left pleural effusions can present as large echo-free spaces that resemble pericardial effusion (movie 2). These can be recognized because they appear as very large posterior spaces often without any anterior component. Generally, in the parasternal long-axis view, pleural effusions extend posterior to the descending thoracic aorta, while pericardial effusions extend anterior to the descending thoracic aorta. Additionally, pericardial effusions only rarely accumulate posterior to the left atrium.

Pericardial thickening and constrictive pericarditis — Although pericardial thickening may be appreciated on echocardiography, CMR and CT are both superior techniques for detecting pericardial thickening and for measuring the thickness [5]. CT is particularly beneficial for identifying pericardial calcifications. (See "Constrictive pericarditis: Diagnostic evaluation", section on 'Initial tests'.)

If pericardial thickening fails to resolve, chronic pericardial thickening with constrictive pericarditis can develop. Like cardiac tamponade, constrictive pericarditis is a continuum of impairment of cardiac function that causes restraint or restriction on ventricular filling sufficient to raise filling pressures and decrease cardiac output or cardiac reserve. One or more of the following TTE findings may be seen in patients with constrictive pericarditis (table 1):

Increased pericardial thickness with or without pericardial adhesion (manifests as the absence of detectable motion between the layers of the pericardium, which may be circumferential or occasionally focal).

Dilatation of the inferior vena cava and hepatic veins (plethora) with absent or diminished inspiratory collapse.

Moderate biatrial enlargement (although severe enlargement is more compatible with restrictive cardiomyopathy).

A sharp halt in ventricular diastolic filling (corresponding to the end of early rapid diastolic filling as noted on Doppler).

Prominent septal bounce with inspiratory motion of the interventricular septum toward the LV.

Abnormal filling of the ventricles during early diastole. An increased early ventricular filling (E) velocity of transtricuspid and transmitral inflow is seen due to the abnormally rapid early diastolic filling associated with the combination of a small ventricular volume and rapid recoil.

Annular early diastolic (E') velocities are lower in constrictive pericarditis secondary to surgery or radiation than in other etiologies but are typically higher than in patients with restrictive cardiomyopathy. The mitral annular lateral/medial E' ratio is reversed in the majority of patients with constrictive pericarditis, with the medial E' velocity being higher than the lateral E' velocity; typically, this is referred to as "annulus reversus."

The propagation velocity of early diastolic transmitral flow on color M-mode is normal or increased [8].

Pronounced respiratory variation in ventricular filling – Mitral inflow peak E wave velocity falls as much as 25 to 40 percent and tricuspid inflow peak E wave velocity greatly increases (>40 to 60 percent) in the first cardiac cycle following inspiration. The respiratory variation in pulmonary venous flow is even more pronounced [9] but may be more technically challenging to obtain. These phenomena, which are manifestations of ventricular interdependence, are not present in either normal subjects or patients with restrictive cardiomyopathy.

Hepatic venous flow reversal increases with expiration, reflecting the ventricular interdependence and the dissociation of intracardiac and intrathoracic pressures.

As with the distinction between cardiac tamponade and pericardial effusion, there can be significant overlap between the findings in frank constriction and those in extensive pericardial thickening without hemodynamic compromise. (See "Constrictive pericarditis: Diagnostic evaluation", section on 'Echocardiography' and "Differentiating constrictive pericarditis and restrictive cardiomyopathy", section on 'Noninvasive testing'.)

Tumors of the pericardium — Localized pericardial thickening or the presence of a pericardial effusion can represent manifestation of primary pericardial malignancy, the result of a pericardial tumor from metastatic disease, or contiguous encroachment of a noncardiac tumor into the pericardial space (movie 8) [10]. Pericardial tumors are almost always associated with an effusion.

If a large tumor invades locally from the lateral chest, it is often possible to appreciate a locally dense area along the lateral border of the heart. The telling characteristic of these masses is often their relative immobility during the cardiac cycle as seen by echocardiography, CMR, or cardiac CT; as the heart abuts these masses, they seem fixed in space and can distort the normal chamber contour. Thoracic magnetic resonance (MR) or CT are often helpful in characterizing mediastinal masses. (See "Cardiac tumors".)

Congenital absence of the pericardium — The normal pericardium exerts considerable influence on cardiac motion, providing stability to the location of the heart in the chest, and limits the dilatation of the chambers. Complete or partial congenital absence of the pericardium is rare and most commonly noted incidentally during surgery or at autopsy [11]. In up to 50 percent of cases, congenital absence of the pericardium is associated with other congenital cardiac defects, including atrial septal defect, patent ductus arteriosus, and tetralogy of Fallot, among others [12]. While most patients have no symptoms, nonspecific symptoms including dyspnea, chest pain, and palpitations are present in others. Partial absence of the pericardium sometimes results in herniation of a chamber through the defect and can be a rare cause of chest pain. There are reports of type A aortic dissection in patients with congenital absence of the pericardium; the mechanism is speculated to be excessive motion of the heart [1].

Partial or complete absence of the pericardium may be suspected but cannot usually be definitively diagnosed by echocardiography, although most TTE findings are nonspecific. The orientation and distance between the transducer and the posterior wall on TTE have been suggested as diagnostic parameters, but in general, thoracic MR and CT are preferred for visualizing the pericardium and confirming the diagnosis [1,13]. Typical findings on echocardiography include:

In patients with complete absence of the pericardium, echocardiography may visualize more of the RV than typically seen on routine left parasternal echocardiogram, which is due to enlargement of the RV, excessive motion of the posterior LV wall, and shift of the heart to the left. These changes may result in paradoxical motion of the interventricular septum. All of these findings mimic RV volume overload as seen in atrial septal defect or tricuspid insufficiency [14].

In patients with partial absence of the pericardium who have herniation of a chamber, TTE may show a wall motion abnormality along the line of demarcation. If the pericardial defect is left sided, it is the left atrial appendage that is most likely involved. However, if a coronary artery is compressed, a true wall motion abnormality may indeed exist [11]. Rare instances of sudden death and acute ischemia resembling an acute ST elevation MI have been reported [1].

No specific treatment is required for most patients with complete congenital absence of the pericardium, as such patients appear to have a normal life expectancy. Partial defects may lead to herniation in which case surgery is indicated. The pericardium can be removed if the defect is large or closed if it is a smaller defect. Surgery in the absence of herniation can be considered if the patient is symptomatic, while occasionally prophylactic closure to prevent future herniation is indicated.

Pericardial cyst — Pericardial cysts (image 6), which typically occur along the right heart border but can occur anywhere, are generally asymptomatic, causing symptoms only if adjacent structures (eg, coronary arteries) are impacted. The primary clinical relevance of pericardial cysts relates to distinguishing the cyst from other cardiac and mediastinal masses. The presence of a pericardial cyst is usually suggested by the chest radiograph.

A pericardial cyst appears as an echo-free space that is more localized and spherical than a pericardial effusion (movie 9) [15]. When TTE images are suboptimal, a pericardial cyst may be more readily visualized with transesophageal echocardiography. In contemporary practice, pericardial cysts are more commonly seen as incidental findings during cross-sectional imaging with thoracic CT or MR, although either MR or CT can be used to confirm a suspected TTE diagnosis of pericardial cyst [16]. Patients generally remain asymptomatic and pericardial cysts remain stable in size over time, but if symptoms arise, surgical intervention may be indicated [16]. (See "Approach to the adult patient with a mediastinal mass", section on 'Middle mediastinal masses'.)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Cardiac tamponade (The Basics)")

Beyond the Basics topics (see "Patient education: Pericarditis (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Transthoracic echocardiography (TTE) is the initial method of choice for evaluating most pericardial diseases, given its ability to rapidly and non-invasively provide both anatomic and physiologic/hemodynamic information. (See 'Introduction' above.)

The normal pericardium consists of two layers: a fibrous outer layer and a serous inner layer. Normally, a small amount of fluid (less than 50 mL) is contained within the closed sac of the serous layer. (See 'Normal anatomy' above.)

When visualized on two-dimensional echocardiography, the layers of the pericardium appear as thin echogenic lines surrounding the myocardium. The normal thickness of the visualized pericardial layers on TTE is less than 3 mm. (See 'Normal appearance on echocardiographic imaging' above.)

In general, TTE should be part of the routine imaging evaluation in the following circumstances: all patients with suspected pericardial disease, including effusion, constrictive pericarditis, or effusive-constrictive pericarditis; all patients with suspected bleeding into the pericardial space (eg, trauma, perforation, post-operative), as a follow-up study to evaluate recurrence of effusion following treatment or to diagnose early constrictive pericarditis, and in patients with pericardial friction rub developing in acute myocardial infarction (MI) accompanied by symptoms such as persistent pain, hypotension, and nausea. (See 'Indications' above.)

Pericardial abnormalities can result from a number of cardiac and systemic conditions, including acute pericarditis, pericardial effusion, cardiac tamponade, constrictive pericarditis, pericardial tumors, and pericardial cysts, among others. Pericardial thickening, loculated effusions, and congenital absence of the pericardium are often better diagnosed using cardiac computed tomography (CT) or cardiovascular magnetic resonance (CMR). (See 'Conditions associated with pericardial pathology' above.)

  1. Shah AB, Kronzon I. Congenital defects of the pericardium: a review. Eur Heart J Cardiovasc Imaging 2015; 16:821.
  2. Cosyns B, Plein S, Nihoyanopoulos P, et al. European Association of Cardiovascular Imaging (EACVI) position paper: Multimodality imaging in pericardial disease. Eur Heart J Cardiovasc Imaging 2015; 16:12.
  3. Horowitz MS, Schultz CS, Stinson EB, et al. Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion. Circulation 1974; 50:239.
  4. American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Society of Echocardiography, American Heart Association, et al. ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography. A Report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, American Society of Echocardiography, American Heart Association, American Society of Nuclear Cardiology, Heart Failure Society of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Critical Care Medicine, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance Endorsed by the American College of Chest Physicians. J Am Coll Cardiol 2011; 57:1126.
  5. Klein AL, Abbara S, Agler DA, et al. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. J Am Soc Echocardiogr 2013; 26:965.
  6. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015; 36:2921.
  7. Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med 2013; 369:1522.
  8. Rajagopalan N, Garcia MJ, Rodriguez L, et al. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol 2001; 87:86.
  9. Sun JP, Abdalla IA, Yang XS, et al. Respiratory variation of mitral and pulmonary venous Doppler flow velocities in constrictive pericarditis before and after pericardiectomy. J Am Soc Echocardiogr 2001; 14:1119.
  10. Chandraratna PA, Aronow WS. Detection of pericardial metastases by cross-section echocardiography. Circulation 1981; 63:197.
  11. Wilson SR, Kronzon I, Machnicki SC, Ruiz CE. A constrained heart: a case of sudden onset unrelenting chest pain. Circulation 2014; 130:1625.
  12. Van Son JA, Danielson GK, Schaff HV, et al. Congenital partial and complete absence of the pericardium. Mayo Clin Proc 1993; 68:743.
  13. Kim MJ, Kim HK, Jung JH, et al. Echocardiographic diagnosis of total or left congenital pericardial absence with positional change. Heart 2017; 103:1203.
  14. Payvandi MN, Kerber RE. Echocardiography in congenital and acquired absence of the pericardium. An echocardiographic mimic of right ventricular volume overload. Circulation 1976; 53:86.
  15. Patel J, Park C, Michaels J, et al. Pericardial cyst: case reports and a literature review. Echocardiography 2004; 21:269.
  16. Alkharabsheh S, Gentry Iii JL, Khayata M, et al. Clinical Features, Natural History, and Management of Pericardial Cysts. Am J Cardiol 2019; 123:159.
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