Abstract
The pericardium is a thin-walled structure composed of two layers, a serous visceral layer (epicardium) and a fibrous parietal layer, both of which surround and protect the heart. Between these layers, up to 50 mL of pericardial fluid normally cushion the heart while the pericardium serves as a barrier to inflammation and infection. Limited epidemiologic data are available for the incidence and prevalence of pericardial disease. Depending on the clinical setting, the etiology of pericardial disease may be attributed to infection, autoimmune, postmyocardial infarction, malignant, metabolic, traumatic, drug-related, congenital, or iatrogenic causes. Transthoracic echocardiography is the first line noninvasive test of choice in patients with suspected pericardial disease. Although the pericardium can be assessed with M-mode, two-dimensional, or three-dimensional echocardiography, two-dimensional echocardiography is most frequently used for assessing pericardial effusions and their hemodynamic significance and also serves as the most cost-effective imaging modality. This chapter reviews the echocardiographic evaluation of the pericardium in various pericardial syndromes: pericardial effusion, pericarditis, pericardial constriction, and other pericardial disorders.
Keywords
constrictive pericarditis, echocardiography, pericardial cyst, pericardial disease, pericardial effusion, pericardial mass, pericarditis
Introduction
The pericardium is a thin-walled structure composed of two layers, a serous visceral layer (epicardium) and a fibrous parietal layer, both of which surround and protect the heart. Between these layers, up to 50 mL of pericardial fluid normally cushion the heart while the pericardium serves as a barrier to inflammation and infection.
Limited epidemiologic data are available for the incidence and prevalence of pericardial disease. Marked variability exists depending on the clinical setting, whether in a developed or developing country and according to the availability of subspecialty care. The etiology of pericardial disease may be attributed to infection, autoimmune, postmyocardial infarction, malignant, metabolic, traumatic, drug-related, congenital, or iatrogenic causes.
Transthoracic echocardiography is the first-line noninvasive test of choice in patients with suspected pericardial disease. The pericardium is typically seen as a bright, linear structure surrounding the heart due to its interface with lung tissue. Although the pericardium can be assessed with M-mode, two-dimensional (2D), or three-dimensional echocardiography, 2D echocardiography is most frequently used for assessing pericardial effusions and their hemodynamic significance and also serves as the most cost-effective imaging modality.
This chapter reviews the echocardiographic evaluation of the pericardium in various pericardial syndromes: pericardial effusion, pericarditis, pericardial constriction, and other pericardial disorders.
Pericardial Fluid
Fluid Characteristics
Pericardial fluid is the serous fluid secreted by the serous layer of the pericardium and is typically echo free by ultrasound. Effusions are often not distributed uniformly in the pericardial space. Hemorrhagic pericardial fluid may serve as a marker of disease (e.g., malignancy) or trauma (e.g., ventricular rupture, coronary artery trauma). Hemopericardium may appear echo free at its onset because echo-free fluid is the same density as the intracardiac blood pool; however, with time the fluid may increase in echodensity, consistent with organizing thrombus. Purulent fluid is consistent with an infectious etiology and associated with elevated fluid protein levels. Such an exudative fluid may also demonstrate stranding or adhesions, consistent with an inflammatory and more complicated disease process. Purulent pericarditis should be managed aggressively with urgent pericardiocentesis, and these effusions are often loculated. Chylous fluid is consistent with trauma or infiltration of the thoracic duct; computed tomography (CT) with and without contrast can aid in the diagnosis.
Effusion Size
The end-diastolic distance of echo-free space between the visceral and parietal pericardium defines the size of a pericardial effusion: trivial (seen only in systole), small (<10 mm), moderate (10–20 mm), large (>20 mm), or very large (>25 mm) ( Fig. 33.1 and 
). Descriptions of effusions should include the size and location of the measurements made. Although there is not a strict correlation between linear dimensions and volume, one may very roughly expect a fluid volume of ≤250 mL from the small effusions, 250–500 mL from the moderate effusions, and greater than 500 mL from pericardiocentesis of large circumferential effusions. Loculated effusions that may occur in the postsurgical setting or secondary to inflammatory disease may not be visible on standard transthoracic echocardiography, and a transesophageal echocardiogram may be necessary.
Distinguishing Features
The position of the descending thoracic aorta relative to the fluid collection is often key to distinguishing a left pleural effusion from a pericardial effusion. Because the visceral pericardium remains closely apposed to the heart muscle itself, fluid anterior to the descending thoracic aorta is more likely to be pericardial, whereas fluid posterior the aorta is more likely to be pleural ( Fig. 33.2 and 
). The descending thoracic aorta can often be identified in apical four-chamber views as well (see Fig. 13.5 ) and used in exactly the same way as a landmark to distinguish pericardial from left pleural effusions.
Epicardial fat sits between the visceral pericardium and the myocardium. Variable amounts can be found over the right ventricle (RV) and the atrioventricular and interventricular grooves. This is often seen as isolated echo-free space anterior to the RV. Increasing the gain settings will show increased texture or brightness relative to the myocardium, which is consistent with epicardial fat. In addition, epicardial fat will move together with the myocardium.
Acute Pericarditis
Acute pericarditis most commonly presents with chest pain that is characterized as sharp, substernal, and pleuritic, with an improvement in symptoms by sitting up and leaning forward. Diagnostic criteria include the presence of two of the following: characteristic chest pain, pericardial rub, widespread ST segment-elevation or PR segment depression on electrocardiogram (ECG), and a new or worsening pericardial effusion.
In the absence of a pericardial rub and ECG changes, imaging of the heart is necessary to make the fourth diagnostic criteria. Although the chest x-ray is likely the first imaging study obtained in a patient with chest pain, the cardiothoracic ratio is often normal in acute pericarditis; the ratio generally only increases once a pericardial effusion is greater than 200–300 mL.
Transthoracic echocardiography will demonstrate the presence of even small pericardial effusions and allow for characterization of the fluid density and size of the effusion. Pericardial effusions may be present without or with tamponade physiology (seen in up to 3% of patients). In some cases, the pericardium may appear bright. The echocardiogram may also appear normal with normal left ventricular function and a trace to small pericardial effusion. Echo imaging may also be helpful in excluding wall motion abnormalities in the setting of myocardial infarction although up to 5% of patients may exhibit wall motion abnormalities with pericarditis, due to concomitant inflammation of the myocardium. Concurrent myopericarditis may present with new focal or global left ventricular dysfunction and elevated cardiac biomarkers.
Several major and minor high-risk features have been associated with an increased risk of subsequent complications from acute pericarditis. Major risk factors include high fever, large pericardial effusion, subacute course, cardiac tamponade, and no response to 7 days of nonsteroidal antiinflammatory drugs (NSAIDs). Minor risk factors include oral anticoagulant therapy, trauma, immunosuppression, and concomitant myocarditis (myopericarditis).
Recurrent Pericarditis
Recurrent pericarditis occurs in 15%–30% of patients after the initial diagnosis. The diagnosis of recurrent pericarditis is made after a 6-week symptom-free interval following the first episode of pericarditis. A patient must also meet the same two of four diagnostic criteria for acute pericarditis.
Echocardiography may demonstrate the presence of a pericardial effusion. Complications such as cardiac tamponade and constriction are less common in recurrent pericarditis. Additional findings may include a septal bounce and other signs of constrictive pericarditis (see later). Cardiac CT may be helpful in assessing pericardial thickness, and delayed gadolinium enhancement with cardiac magnetic resonance imaging (MRI) may be helpful in demonstrating inflammation of the pericardium.
Pericardial Tamponade
The hemodynamic response to a pericardial effusion is most closely related to the speed with which the fluid accumulates, the distensibility of the pericardium, and the filling pressures and compliance of the cardiac chambers rather than the size or total volume. Pericardial tamponade describes the state in which excessive pericardial fluid with elevated intrapericardial pressures limits cardiac filling. As the amount of pericardial fluid increases, pericardial pressure rises, which results in a compensatory rise in pulmonary and systemic venous pressures to maintain cardiac output. Eventually, the compensatory mechanisms fail and preload can no longer support cardiac filling.
Two-dimensional echocardiography will often demonstrate a large pericardial effusion in tamponade. Irrespective of the size of the effusion, the most worrisome signs include the presence of dilated hepatic veins and a dilated inferior vena cava (see Fig. 13.4 ), which together represent the presence of elevated systemic venous pressures. These findings together with a small left ventricle (LV) suggest the presence of a reduction in stroke volume and cardiac output. Additional findings of elevated intrapericardial pressure include early diastolic collapse of the RV and inversion of the right atrium for greater than one-third of the cardiac cycle (see Fig. 13.6 and 
). Collapse of the atria occurs near the peak of the R wave, whereas collapse of the ventricles occurs at the end of the T wave in early diastole. Due to thin wall of the right atrium, collapse of the chamber may be seen in patients without tamponade; however, if the duration of RA inversion is greater than one-third of the cardiac cycle, this finding has been described to be 100% sensitive and specific for cardiac tamponade. The severity of tamponade increases with the duration of chamber collapse. The right-sided chambers are most susceptible to compression due to its lower filling pressures. Examples are shown and discussed in Chapter 13 .
M-mode echocardiography is particularly well suited to demonstrate changes in chamber dimensions, right-sided chamber collapse, and interventricular dependence in relation to respiratory variation, in part due to the increase in temporal resolution with this technique ( Fig. 33.3 ; see also Fig. 13.6 ). These patients are often tachycardic, so an M-mode cursor through the chamber or wall of interest can aid in the judgment of duration and timing of chamber collapse. As fluid accumulates in the pericardial space, intrapericardial pressure rises and hemodynamics mimic constrictive physiology. With inspiration, increased filling to the RV results in a leftward shift of the ventricular septum and decreased filling of the LV. With expiration, increased filling to the LV results in a reciprocal rightward shift of the ventricular septum and decreased filling of the RV. This relationship can be appreciated on M-mode and 2D echocardiography.
Doppler echocardiographic findings include exaggerated respiratory variation in mitral (>25%) and tricuspid (>40%) inflow velocities due to the ventricular interdependence that develops as intrapericardial pressure rises (as in Fig. 13.7 ). The respiratory changes are highest on the first beats of inspiration and expiration. The consensus for calculation is (expiration-inspiration)/expiration for both mitral and tricuspid inflow. Respiratory variation can also be demonstrated in LV outflow tract and RV outflow tract flows. In addition, hepatic vein velocities will be reduced, reflecting the reduction in cardiac filling. As the degree of tamponade increases, blunting or reversal of diastolic flow in expiration may be appreciated in the hepatic veins.
Special consideration should be given to patients with history of elevated right-sided chamber pressures prior to the development of the pericardial effusion. In this setting, right-sided chamber collapse may occur later in the development of tamponade physiology because it will take an even greater intrapericardial pressure to collapse the right-sided chambers in diastole. Similarly, low intracardiac pressures, such as in hypovolemia, may result in earlier collapse of right-sided chambers. In those with loculated pericardial effusions, attention should be given to the left-sided chambers and any cardiac chambers adjacent to the effusion (see 
).
Pericardial constriction and tamponade share many similar characteristics, including echocardiographic findings ( Table 33.1 ). Aside from the presence of a pericardial effusion, clinical characteristics seen at the bedside and hemodynamics in the cardiac catheterization lab can help distinguish the two diagnoses.
| Pericardial Constriction | Tamponade | |
|---|---|---|
| Two-Dimensional Echo Findings | ||
| Pericardial space | ± Effusion | Effusion |
| Inferior vena cava | Dilated, diminished collapse | Dilated, diminished collapse |
| Septal position | Ventricular interdependence (Septal shift, varies with respiration) | Ventricular interdependence (Septal shift, varies with respiration) |
| Echo Doppler Findings | ||
| Respiratory variation in E wave (mitral) | >25% | >25% |
| Respiratory variation in E wave (tricuspid) | >40% | >40% |
| Hepatic vein flow | Diastolic reversal | Diastolic reversal |
| M-mode Findings | ||
| Septal position | Ventricular interdependence (Septal shift, varies with respiration) | Ventricular interdependence (Septal shift, varies with respiration) |
| Septal bounce | ||
| Left ventricle posterior wall flattening | ||
| Clinical Findings | ||
| Jugular venous pressure | Elevated | Elevated |
| Pulsus paradoxus | Uncommon | Common |
| Kussmaul sign | Present | Absent |
| Cardiac Catheterization Findings | ||
| Y descent | Exaggerated (Prominent early diastolic filling) | Blunted (Prominent systolic filling) |
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