DOI: 10.1148/rg.276065002
RadioGraphics 2007;27:1595-1610
© RSNA, 2007
Imaging Findings in Cardiac Tamponade with Emphasis on CT1
C. Santiago Restrepo, MD,
Diego F. Lemos, MD,
Julio A. Lemos, MD,
Enrique Velasquez, MD,
Lisa Diethelm, MD,
Ty A. Ovella, MD,
Santiago Martinez, MD,
Jorge Carrillo, MD,
Rogelio Moncada, MD, and
Jeffrey S. Klein, MD
1 From the Department of Radiology, University of Texas Health Sciences Center, San Antonio (C.S.R.); the Department of Radiology, Fletcher Allen Health Care and University of Vermont, FAHC/MCHV Campus, Patrick 1, Room 117, 111 Colchester Ave, Burlington, VT 05401-1473 (D.F.L., J.A.L., J.S.K.); the Departments of Cardiology (E.V.) and Radiology (T.A.O., R.M.), Louisiana State University Health Science Center, New Orleans; the Department of Radiology, Ochsner Clinic Foundation, New Orleans (L.D.); the Department of Radiology, Duke University, Durham, NC (S.M.); and the Department of Radiology, Universidad Nacional de Colombia, Bogotá (J.C.). Recipient of a Certificate of Merit award for an education exhibit at the 2004 RSNA Annual Meeting. Received January 10, 2006; revision requested March 22; final revision received May 15, 2007; accepted May 21. All authors have no financial relationships to disclose.
Address correspondence to D.F.L. (e-mail: Diego.Lemos{at}vtmednet.org).
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Abstract
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Cardiac tamponade is a life-threatening condition that results from slow or rapid heart compression secondary to accumulation of fluid, pus, blood, gas, or tissue within the pericardial cavity. This condition can be associated with multiple causes including trauma, inflammation, scarring, or neoplastic involvement of the pericardial space among others. The main pathophysiologic event leading to tamponade is an increase in intrapericardial pressure sufficient to compress the heart with resultant hemodynamic impairment, which leads to limited cardiac inflow, decreased stroke volume, and reduced blood pressure. These events result in diminished cardiac output, which manifests clinically as a distinctive form of cardiogenic shock. Although cardiac tamponade is a clinical diagnosis, imaging studies play an important role in assessment and possible therapeutic intervention. Computed tomographic (CT) findings associated with cardiac tamponade include pericardial effusion, usually large, with distention of the superior and inferior venae cavae; reflux of contrast material into the azygos vein and inferior vena cava; deformity and compression of the cardiac chambers and other intrapericardial structures; and angulation or bowing of the interventricular septum. Familiarity with the clinical and pathophysiologic features of cardiac tamponade and correlation with the associated CT findings are essential for early and accurate diagnosis.
© RSNA, 2007
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LEARNING OBJECTIVES FOR TEST 2
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After reading this article and taking the test, the reader will be able to:
- Describe the pathophysiology and clinical manifestations of cardiac tamponade.
- List the imaging findings of developing or impending cardiac tamponade and its differential diagnostic considerations.
- Discuss how the underlying pathophysiologic events correlate with the imaging manifestations of cardiac tamponade.
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Introduction
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Cardiac tamponade is one condition in the spectrum of pericardial compressive syndromes. When material accumulates within the pericardial cavity or when the pericardium becomes scarred, thickened, or inelastic, one of three pericardial compressive syndromes may develop. These include cardiac tamponade, constrictive pericarditis (the result of scarring and consequent loss of elasticity of the pericardium), and effusive-constrictive pericarditis (a variant characterized by constrictive physiology with a coexisting pericardial effusion, usually with tamponade) (1).
Cardiac tamponade is a hemodynamic state that results from the slow or rapid accumulation of fluid, pus, blood, gas, or benign or malignant neoplastic tissue within the pericardial cavity. It can be acute or subacute, but other variants including low pressure (occult) and regional tamponade may also occur. The incremental increase in the intrapericardial volume raises the intrapericardial pressure, resulting in compression of the heart, which restricts the filling of the cardiac chambers with resultant severe hemodynamic impairment and eventually reduced cardiac output (1–3).
Echocardiography is considered the imaging technique of choice for assessment of pericardial effusion and tamponade. However, in equivocal cases or when echocardiography is not feasible, additional imaging studies including computed tomography (CT) or magnetic resonance (MR) are necessary (Fig 1). Cross-sectional techniques may provide morphologic signs of developing or impending tamponade that have significant hemodynamic correlates. Furthermore, additional information with assessment of the entire chest including associated abnormalities in the mediastinum, lungs, and adjacent structures is possible due to the larger field of view compared with that of echocardiography. Radiologists should be aware of the imaging findings of tamponade with cross-sectional techniques in order to allow early diagnosis and prompt, life-saving interventions.
In this article, we briefly review the anatomy, pathophysiology, and clinical manifestations of cardiac tamponade, with a particular focus on the CT findings of this life-threatening condition.
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Anatomy
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The pericardium is a double-walled sac consisting of an external fibrosa layer and beneath it a serosa layer. The serosa is a complete closed sac that reflects on itself and covers the heart with some extensions to enclose portions of the juxtacardiac great vessels and the inner aspect of the fibrosa. The serosa directly covering the surface of the heart is the visceral pericardium (also known as the epicardium). The fibrosa together with the reflections of the serosa internally attached to it is known as the parietal pericardium. The space between the visceral and parietal pericardium is the pericardial cavity. This pericardial cavity normally contains a small amount of pericardial fluid (15–50 mL) produced by the mesothelial cells that line the serosa. A number of pericardial sinuses and recesses between the reflections of the pericardium serve as a potential space to accommodate a limited amount of additional pericardial fluid, which contributes and augments the pericardial reserve volume (4–7).
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Pathophysiology
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Cardiac tamponade is a condition characterized hemodynamically by decreased intracardiac volumes and increased diastolic filling pressures. Increase of the intrapericardial pressure producing external cardiac compression is the critical event in the development of tamponade. Under normal physiologic conditions, the intrapericardial pressure is equal to intrapleural pressure and therefore negative. The elevation of the intrapericardial pressure is the result of rapid or slow accumulation of fluid, gas, or tissue within the pericardial cavity. As the pericardial contents initially increase, the pericardial space accommodates the expanding volume of material without an increase in pressure or compromise of the cardiac chambers until the limit of the pericardial reserve volume is reached. As the pericardial contents continue increasing, the limit of pericardial stretch is exceeded and there begins to be compromise of the cardiac chambers, which become smaller. This effectively reduces myocardial diastolic compliance and therefore limits blood inflow, ultimately leading to equalization of the mean diastolic pericardial and cardiac chamber pressures (Fig 2) (3).
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Figure 2. Pericardial pressure-volume curves. As the pericardial effusion initially increases, the pericardial space accommodates the expanding volume of fluid without a significant increase in pressure or compromise of the cardiac chambers until the limit of the pericardial reserve volume is reached. Left: In rapidly increasing pericardial effusion, after the pericardial reserve volume limit is reached, the limit of parietal pericardial stretch is then quickly exceeded even with as little as 200 mL of fluid, causing a steep rise in pressure with beginning of compromise of the cardiac chambers, which become smaller. The curve becomes even steeper as smaller increments in fluid cause a disproportionate increase in the pericardial pressure; this process effectively reduces myocardial diastolic compliance and therefore limits blood inflow, ultimately leading to equalization of the mean diastolic pericardial and cardiac chamber pressures, which results in decrease of stroke volume, reduction of arterial blood pressure, diminished coronary blood flow, and finally reduced cardiac output. Right: In pericardial effusions with a slower filling rate, it takes longer to exceed the limit of pericardial stretch and the pericardium can accommodate volumes as large as 1500 mL without hemodynamic compromise; however, once the limit of pericardial stretch is exceeded, even small increments in pericardial volume may provoke full-blown tamponade (3).
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The initial effects of the increase in pericardial pressure are on the thinner, more compliant right cardiac chambers and eventually for all chambers with limited diastolic chamber filling, which results in decreased stroke volume, reduction of arterial blood pressure, diminished coronary blood flow, and finally reduced cardiac output (3,8,9).
The rate of accumulation is more significant in establishing cardiac tamponade than the ultimate size or composition of the pericardial contents (10). In the acute setting, the pericardium is relatively stiff and noncompliant. Accordingly, acute or rapidly developing pericardial effusions can abruptly increase the intrapericardial pressure and produce cardiac tamponade with as little as 100–200 mL of pericardial fluid. On the other hand, over time the pericardium can stretch and become more compliant. Therefore, slow or gradual accumulation of pericardial fluid of up to 1000–1500 mL can be tolerated without hemodynamic impairment (11). However, once the pericardium has maximally distended to accommodate the increasing pericardial contents, even small increments in intrapericardial volume will eventually result in acute tamponade due to an abrupt increase in intrapericardial pressure (2,3,10–12). Note that an abnormally thickened pericardium may have a much lower threshold for increases in pressure that lead to tamponade due to its inability to expand normally to accommodate an increasing intrapericardial volume.
The term effusive-constrictive pericarditis refers to an uncommon pericardial syndrome characterized by concomitant tamponade and constriction. The tamponade is caused by tense pericardial effusion; the constriction is caused by scarring or calcification of the visceral pericardium or epicardium. Patients with effusive-constrictive pericarditis may be erroneously believed to have only tamponade; however, in the former entity the central venous pressure typically remains elevated after drainage of the pericardial effusion (13).
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Clinical Findings
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Although cardiac tamponade is a clinical diagnosis, most signs and symptoms are nonspecific when analyzed individually. However, these manifestations may strongly suggest tamponade when they occur simultaneously or when considered together in the proper clinical scenario. Tachycardia is almost always present with some exceptions (ie, bradycardic patients in uremia and those with hypothyroidism). Owing to the markedly diminished intracardiac volumes, the stroke volume is reduced, triggering a cascade of compensatory mechanisms to maintain cardiac output and blood pressure including sympathetic and catecholamine stimulation, which result in increased contractility, tachycardia, and vasoconstriction (3).
Clinically significant tamponade frequently produces hypotension. In rapidly developing tamponade, patients usually are in shock with jugular venous distention, which is a key finding in differentiating it from other forms of endovascular collapse. Signs of poor peripheral perfusion include cool legs, arms, ears, and nose, as well as peripheral cyanosis (3,12). The Beck triad (muffled heart sounds, hypotension, and jugular venous distention) strongly suggests tamponade but is present in only a minority of patients (14). Pulsus paradoxus (an exaggerated fall in systolic blood pressure of 10 mm Hg or more during inspiration) is one of the most useful physical findings and an ominous sign of impending hemodynamic collapse, but again it is nonspecific and may be blunted, absent, or difficult to reproduce (12). Other conditions that can also produce pulsus paradoxus include massive pulmonary thromboembolism, obstructive lung disease, profound hemorrhagic shock, and other forms of severe hypotension (3).
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Imaging Findings
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Chest Radiography
Conventional radiographs of the chest in patients with cardiac tamponade may demonstrate an enlarged cardiac silhouette with or without an epicardial fat pad sign suggesting a pericardial effusion; the lungs are typically clear (Fig 3) (3,8,15). However, chest radiographs may not be useful early in the course of the process, since at least 200 mL of pericardial fluid must accumulate before visible enlargement of the cardiac silhouette occurs (3). Cases of acute cardiac tamponade after blunt chest trauma with a normal-size heart on chest radiographs have been reported in the literature (16,17).
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Figure 3a. Cardiac tamponade secondary to tuberculosis in a 32-year-old man with acquired immunodeficiency syndrome. (a) Chest radiograph shows significant enlargement of the cardiac silhouette with the characteristic "water bottle" appearance. (b) Axial nonenhanced CT image of the chest shows a large pericardial effusion flattening the anterior cardiac contour.
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Figure 3b. Cardiac tamponade secondary to tuberculosis in a 32-year-old man with acquired immunodeficiency syndrome. (a) Chest radiograph shows significant enlargement of the cardiac silhouette with the characteristic "water bottle" appearance. (b) Axial nonenhanced CT image of the chest shows a large pericardial effusion flattening the anterior cardiac contour.
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In patients with pneumopericardium, chest radiographs typically show the heart surrounded partially or completely by air with a sharply delineated pericardium outlined by lucency on either side (Fig 4) (17). In patients with tamponade due to pneumopericardium, termed tension pneumopericardium, a substantial decrease in the size of the cardiac silhouette may be observed on radiographs, the so-called small heart sign (Fig 5) (17–19). In addition, chest radiographs may show not only pneumopericardium but also the presence of coexistent pneumothorax or pneumomediastinum. Traumatic or congenital communications (ie, fenestrations) between the pleural space and the pericardium with a one-way valve mechanism may have a role in the development of tension pneumopericardium, particularly if there is associated pneumothorax without pneumomediastinum and no evidence of any penetrating pericardial wound (20).
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Figure 4. Cardiac tamponade in a newborn with respiratory distress syndrome who developed pneumopericardium associated with barotrauma from mechanical ventilation. Chest radiograph shows pneumopericardium with cardiac tamponade.
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Figure 5. Pneumopericardium with cardiac tamponade in an adult patient with blunt thoracic trauma. Chest radiograph shows a sharply delineated pericardium (arrowheads) outlined by air on both sides. The small heart sign suggests the presence of tension pneumopericardium.
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Echocardiography
Echocardiography is the imaging technique of choice for diagnosis of pericardial effusion and cardiac tamponade. It is readily available and portable, lacks ionizing radiation, and is highly sensitive for detection of pericardial effusion. It is also very specific for diagnosis of pericardial tamponade if the characteristic imaging findings are identified. Some of the echocardiographic findings described in cardiac tamponade include cardiac chamber compression, inferior vena cava (IVC) plethora, Doppler flow velocity paradoxus, compression of the pulmonary trunk, compression of the thoracic IVC, paradoxical motion of the interventricular septum, and swinging motion of the heart in the pericardial sac (Fig 6) (3,8,21–25).
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Figure 6a. Cardiac tamponade in a 50-year-old man with a 3-week history of malaise and dyspnea. (a) Parasternal short-axis echocardiographic view shows a large circumferential pericardial effusion (PE) surrounding the left ventricle (LV). (b) Subcostal long-axis echocardiographic view shows diastolic collapse of the right atrium (RA) as well as a dilated and plethoric IVC. PE = pericardial effusion. Cardiac arrest later developed, and the patient required emergent pericardiocentesis.
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Figure 6b. Cardiac tamponade in a 50-year-old man with a 3-week history of malaise and dyspnea. (a) Parasternal short-axis echocardiographic view shows a large circumferential pericardial effusion (PE) surrounding the left ventricle (LV). (b) Subcostal long-axis echocardiographic view shows diastolic collapse of the right atrium (RA) as well as a dilated and plethoric IVC. PE = pericardial effusion. Cardiac arrest later developed, and the patient required emergent pericardiocentesis.
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As mentioned earlier, the thinner more compliant right-sided chambers are usually the first to be compressed in the setting of cardiac tamponade. Right atrial and right ventricular collapse are the most commonly used clues for tamponade at echocardiography; however, neither of them is 100% sensitive or specific for tamponade (3,8).
Right atrial collapse, which occurs in late diastole or early systole, reflects increased intrapericardial pressure inverting the right atrial wall inward when the right atrial pressure is lowest. This echocardiographic sign has a reported sensitivity of 55%–60% and specificity of 50%–68% for tamponade. Right atrial collapse is more specific if the inward movement lasts for at least 30% of the cardiac cycle. Right ventricular collapse, which occurs in early diastole, is a less sensitive (38%–48%) but more specific (84%–100%) finding for cardiac tamponade; however, it has been considered a late sign. Collapse of the left atrium, which takes place in late diastole, may occur in approximately 25% of patients and is highly specific for tamponade. Left ventricular collapse also has low sensitivity and usually occurs under specific circumstances such as localized postsurgical tamponade (3,8,21,22).
Another echocardiographic sign for tamponade is a distended IVC or IVC plethora. Normally, the proximal IVC decreases by more than 50% in diameter after a deep inspiration or a sniff. In tamponade, by definition the right atrial pressure is elevated and the IVC typically is distended and will not decrease in diameter with these maneuvers. However, IVC plethora is not a specific finding for tamponade and may be present in other conditions causing elevated right atrial pressure (8).
Abnormal Doppler flow has a good correlation with clinical features of tamponade, with a higher sensitivity (75%) than right ventricular collapse and a much higher specificity (91%) than right atrial collapse (23). Marked respiratory variation in Doppler velocities, the so-called Doppler flow velocity paradoxus, is a pattern of reciprocal variation in the left- and right-sided transvalvular inflow velocities. Normally, there is no significant respiratory variation in early diastolic filling velocities across the tricuspid and mitral valves. In tamponade, however, there may be an exaggerated "paradoxical" increase in right-sided inflow velocities with an exaggerated decrease in left-sided inflow velocities (8,24). Unfortunately, this "flow velocity paradoxus" is not specific for tamponade either.
Other recently described echocardiographic signs in tamponade include compression of two intrapericardial structures, the pulmonary trunk and the thoracic IVC. The pulmonary trunk is an entirely intrapericardial short and wide vessel. The short intrathoracic segment of the IVC is extrapericardial in its posterior aspect but is covered by pericardium on its anterior aspect. This is the reason why in pericardial effusion with tamponade, there is indentation of the right atrium at the level of the IVC junction anteriorly but not posteriorly (25).
One mechanism of pulsus paradoxus is also visible at echocardiography when both the ventricular and atrial septa move sharply to the left with an increase in right chamber volumes at the expense of the left chambers. The reverse occurs in expiration. This paradoxical motion of the septa occurs because each side of the heart fills at the expense of the other due to the fixed intrapericardial volume (8,12).
The mechanism of electrical alternans, an electrocardiographic finding, is due to the swinging motion of the heart within the pericardial sac, another visible echocardiographic sign. Typically, the extremes of oscillation of the heart can be seen, particularly in large effusions. Unfortunately, while electrical alternans is a highly specific sign of tamponade on an electrocardiogram, a swinging heart is neither sensitive nor specific for tamponade at echocardiography (3,8,12).
Computed Tomography
Echocardiography remains the primary method of evaluating pericardial disease, in particular pericardial effusion. An advantage of CT of the chest over echocardiography in the evaluation of suspected pericardial disease is the larger field of view inherent in CT, which allows assessment of the entire chest and detection of associated abnormalities in the mediastinum, lungs, and adjacent structures. CT is also less operator dependent, and owing to the improved temporal resolution of multidetector CT, the acquisition of high-quality motion-free images of the pericardium is possible, particularly in patients with limited breath-hold capacity. In addition, multidetector CT scanners may offer retrospective cardiac gating, thus allowing acquisition of cine CT images, which provide valuable information about the function and dynamics of the heart and pericardium. Another advantage of CT over other modalities is its ability to demonstrate pericardial calcification, allowing measurement of its thickness, location, and extent (6–8).
Some of the reported limitations of echocardiography are generally not present with CT, including the high rate of false-positive findings due to adjacent pathologic conditions that may simulate pericardial effusions (ie, pleural effusions, lower lobe atelectasis, pericardial and intracardiac masses, or other mediastinal lesions). Other limitations include the difficulty of identifying clotting or clots within the pericardium at echocardiography as well as differentiation of small fluid collections from pericardial thickening, differentiation of fluid in the anterior and posterior spaces around the heart from epicardial fat, and identification of loculations in complex pericardial collections (8,26,27).
CT provides valuable information about the possible nature of pericardial effusions based on the attenuation measurements of the collection. Pericardial fluid with relatively low attenuation values close to that of water likely represents a simple serous effusion from underlying heart failure, renal failure, or nonhemorrhagic carcinomatous involvement. Attenuation values greater than that of water suggest hemopericardium, malignancy, purulent exudates, or myxedematous effusion associated with hypothyroidism. Low attenuation values with measurements close to that of fat have been reported in cases of chylopericardium (28,29).
CT also allows differentiation of pericardial thickening from pericardial fluid owing to the occasional presence of nodular areas of increased attenuation in pericardial thickening, the typical anterior location of the thickened pericardium, lack of change at decubitus positioning, and pericardial enhancement with administration of contrast material (26). Occasionally, this differentiation can be difficult, particularly in cases of small pericardial collections (27,28).
Some of the reported CT findings in tamponade include enlargement of the superior vena cava with a diameter similar to or greater than that of the adjacent thoracic aorta (Fig 7), enlargement of the IVC with a diameter greater than twice that of the adjacent abdominal aorta (Fig 8), periportal lymphedema (Fig 9), reflux of contrast material within the IVC (Fig 10), reflux of contrast material within the azygos vein, and enlargement of hepatic and renal veins (10,30–34). Unfortunately these findings seen individually are not specific for tamponade, but the constellation of findings should strongly suggest the diagnosis, particularly in the presence of a large pericardial effusion.
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Figure 7. Dilatation of the superior vena cava in a 74-year-old woman with cardiac tamponade after revascularization surgery. Axial contrast-enhanced CT image obtained inferior to the aortic arch shows an abnormally dilated superior vena cava (straight arrow) with a diameter similar to that of the adjacent aorta (arrowhead). There is also reflux of contrast material within the azygos vein (curved arrow).
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Figure 8. Dilatation of the IVC in a 20-year-old man with a pericardial effusion and signs and symptoms of cardiac tamponade. Contrast-enhanced CT image of the chest shows an abnormally dilated IVC (straight arrow) with a diameter greater than twice that of the adjacent abdominal aorta (arrowhead). The coronary sinus (curved arrow) also appears prominent.
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Figure 9a. Cardiac tamponade in a 23-year-old man with a history of intravenous drug abuse who presented with chest pain and shortness of breath. (a) Contrast-enhanced CT image obtained at the level of the ventricles shows a large pericardial effusion deforming the cardiac contours. Note the dilated IVC (arrow) and the slightly dilated azygos vein (arrowhead). The fluid was an inflammatory exudate, and cultures were negative. (b) Contrast-enhanced CT image of the upper abdomen shows periportal fluid (arrows) due to distended periportal lymphatic vessels.
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Figure 9b. Cardiac tamponade in a 23-year-old man with a history of intravenous drug abuse who presented with chest pain and shortness of breath. (a) Contrast-enhanced CT image obtained at the level of the ventricles shows a large pericardial effusion deforming the cardiac contours. Note the dilated IVC (arrow) and the slightly dilated azygos vein (arrowhead). The fluid was an inflammatory exudate, and cultures were negative. (b) Contrast-enhanced CT image of the upper abdomen shows periportal fluid (arrows) due to distended periportal lymphatic vessels.
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Figure 10. Cardiac tamponade in a 59-year-old man who presented to the emergency department with shortness of breath. Axial CT image shows a large pericardial effusion with a compressed small heart and reflux of contrast material into the IVC (arrow). A moderate-sized right pleural effusion and very small left pleural effusion are also seen. The patient had clinical and hemodynamic findings consistent with pericardial tamponade.
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For example, periportal lymphatic distention or lymphedema has been described not only in cardiac tamponade but also in patients with chronic congestive heart failure, blunt abdominal trauma with or without liver injuries, cirrhosis, hepatitis, liver transplants, and hepatic or retroperitoneal malignancies (34,35). Similarly, reflux of contrast material into the IVC occurs not only in the setting of cardiac tamponade but can be seen in individuals with intrinsic cardiac disease such as tricuspid regurgitation, patients with hypovolemic or cardiogenic shock, and those with pulmonary embolism, among others (32,33,36). Azygos vein reflux can occur in a variety of conditions that raise the central venous pressure, including massive pulmonary embolism, cor pulmonale, ischemic right-sided heart failure, pulmonary arterial hypertension, tumoral obstruction of the main pulmonary artery, and bilateral pneumothoraces, as well as in patients with acute respiratory distress syndrome receiving positive pressure ventilation (32,33,37,38).
An additional CT finding that should suggest pericardial tamponade is the so-called flattened heart sign (39). This sign occurs when the increased intrapericardial pressure is sufficient to produce transient reversal of the transmural left ventricular pressure during diastole, thereby producing a change in the contour of the anterior aspect of the heart with resultant hemodynamic changes (39). This CT sign is characterized by flattening of the anterior surface of the heart with decreased anteroposterior diameter and can occur secondary to the presence of fluid (Fig 11), air (Fig 12), or tissue (Fig 13) compressing the cardiac chambers (39). In severe cases, inversion with concave chamber deformity may be seen (Fig 14). Compressive deformity of the cardiac chambers, particularly the thinner and more compliant right-sided chambers, typically manifests at CT as straightening of the right cardiac contour (Fig 15).
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Figure 11. Cardiac tamponade in a 44-year-old man with a history of lung cancer who presented with progressive shortness of breath, tachycardia, and tachypnea. Axial nonenhanced CT image obtained at the level of the ventricles shows a pericardial effusion, which produces abnormal flattening of the anterior surface of the heart (arrowhead).
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Figure 12. Pneumopericardium with tamponade physiology in a 28-year-old man after blunt trauma. Contrast-enhanced CT image obtained at the level of the ventricles shows pneumopericardium with compression of the anterior surface of the heart (black arrowheads). There is associated left pneumothorax (white arrowhead). Left basilar atelectasis and a left pleural effusion are also seen.
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Figure 13. Immunoblastic T-cell lymphoma with pleural and pericardial involvement in a 30-year-old man who presented with cardiac tamponade. Contrast-enhanced CT image shows decreased anterior-posterior diameter of the heart due to significant compression of the anterior (arrow) and posterior (arrowhead) cardiac surfaces by neoplastic tissue. There are associated bilateral pleural effusions.
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Figure 14. Non-Hodgkin lymphoma in a 62-year-old man who presented with cardiac tamponade. Nonenhanced CT image shows abnormal concave deformity of the anterior wall of the right ventricle, compression of the anterior epicardial fat (arrowhead), and a moderate-sized pericardial effusion. The patient died shortly after this examination was performed.
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Figure 15. Cardiac tamponade in a 34-year-old man with acquired immunodeficiency syndrome. Contrast-enhanced CT image shows a pericardial effusion and bilateral pleural fluid collections. Note the straightening of the anterior and right lateral cardiac contours (arrow), as well as the collapsed anterior right ventricle (arrowhead).
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Compression of the coronary sinus (an intrapericardial structure) may be another sign of impending cardiac tamponade. This is a similar phenomenon to the previously described compression of the pulmonary trunk (an entirely intrapericardial vessel) and the short intrathoracic segment of the IVC (which is extrapericardial posteriorly but is covered by pericardium anteriorly). This sign was appreciated in a patient with coronary perforation during a percutaneous coronary intervention with resultant tamponade (40). Although this sign was documented with angiography, CT can also demonstrate an abnormal coronary sinus; therefore, the radiologist should be able to identify this finding and its significance in the proper scenario, particularly in the presence of simultaneous pericardial effusion.
Another CT finding that can be observed in cardiac tamponade is angulation or bowing of the interventricular septum. This CT finding correlates with the paradoxical motion of the septum frequently observed on echocardiograms of patients with tamponade physiology (8,41,42) (Fig 16). However, this finding is not specific for tamponade, as septal shifting can be seen in other processes that occur with either pressure or volume overload of the right ventricle or both. Besides cardiac tamponade, septal "bounce" has been reported in other conditions including constrictive pericardial disease (41–44), as well as in conditions producing right ventricular dysfunction such as massive pulmonary embolism (45,46).
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Figure 16. Cardiac tamponade in a 38-year-old man after a motor vehicle collision. Contrast-enhanced CT image shows abnormal bowing of the interventricular septum (arrowhead) toward the left ventricle. There is an associated large pericardial effusion.
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Specific Causes of Pericardial Tamponade as Demonstrated at CT
As previously mentioned, CT may help in the differentiation of malignant from benign causes of pericardial effusion. Malignant pericardial disease is suggested by several CT criteria, including pericardial effusions with high CT attenuation values (usually >20 HU), localized or diffuse pericardial thickening, masses arising from or contiguous with the pericardium, and obliteration of the normal tissue planes between a paracardiac mass and the heart or pericardium (47) (Figs 17, 18). Note that not all cases of tamponade in the setting of malignant pericardial disease are due to associated effusion, as hemodynamic impairment can occur in patients with pericardial malignancy as a result of compression of cardiac chambers by tumor masses alone (Fig 19).
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Figure 17a. Cardiac tamponade in a 61-year-old man with a pericardial metastasis. (a) Contrast-enhanced CT image obtained at the level of the ventricles shows a large pericardial fluid collection with a single solid metastatic nodule (arrowhead). A left pleural fluid collection is also noted. (b) Contrast-enhanced CT image shows periportal fluid in the porta hepatis (curved arrow) and a hypoattenuating collar surrounding the intrahepatic portion of a distended IVC. The distended IVC demonstrates a fluid–contrast material level (straight arrow), which is due to refluxed contrast material from the right atrium layering within the dependent portion of the IVC. Note the small liver metastases and left paraaortic node metastasis.
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Figure 17b. Cardiac tamponade in a 61-year-old man with a pericardial metastasis. (a) Contrast-enhanced CT image obtained at the level of the ventricles shows a large pericardial fluid collection with a single solid metastatic nodule (arrowhead). A left pleural fluid collection is also noted. (b) Contrast-enhanced CT image shows periportal fluid in the porta hepatis (curved arrow) and a hypoattenuating collar surrounding the intrahepatic portion of a distended IVC. The distended IVC demonstrates a fluid–contrast material level (straight arrow), which is due to refluxed contrast material from the right atrium layering within the dependent portion of the IVC. Note the small liver metastases and left paraaortic node metastasis.
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Figure 18. Cardiac tamponade in a 65-year-old woman with a history of Merkel cell carcinoma of the skin and a metastasis to the pericardium. Contrast-enhanced CT image shows a large pericardium-based mass (arrowhead) compressing the anterior surface of the heart. A moderate amount of pericardial fluid (arrow) and large left pleural fluid collections are also noted.
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Figure 19. Pericardial metastasis in a 62-year-old woman who presented with tamponade physiology. Contrast-enhanced CT image shows innumerable solid nodular metastatic deposits projecting within the pericardial cavity. Note the absence of pericardial fluid. There are bilateral pleural fluid collections.
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There is a wide spectrum of cardiac pathologic conditions associated with tamponade, including free-wall cardiac rupture after myocardial infarction (48), rupture of a ventricular aneurysm (49), rupture of a coronary aneurysm (50), complications after thrombolytic therapy such as hemopericardium (51) and ventricular wall hematoma (52), Dressler syndrome (53), complications of endocarditis (54), and cardiac neoplasms (55).
Trauma can produce cardiac tamponade by several different mechanisms. Penetrating trauma can result in hemopericardium and tamponade. A posttraumatic anterior mediastinal hematoma, such as may be seen after blunt injury with sternal fracture, or a postsurgical hematoma after coronary artery bypass surgery (56,57) (Fig 20) are additional causes. Rarely, intrapericardial herniation of subdiaphragmatic intestinal contents after blunt abdominal trauma can compress the heart and produce cardiac tamponade (58,59) (Fig 21).
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Figure 20. Extracardiac tamponade in a 62-year-old man with coronary artery disease who underwent coronary artery bypass graft surgery. He presented 2 weeks after the intervention with clinical findings suggestive of tamponade. Contrast-enhanced CT image shows an anterior mediastinal fluid collection (arrowheads) that compresses and deforms the anterior surface of the heart, predominantly the right ventricle.
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Figure 21a. Pericardial tamponade in a 63-year-old woman with a delayed posttraumatic diaphragmatic hernia. (a) Contrast-enhanced CT image obtained at the level of the ventricles shows intrapericardial herniation of the colon (arrows), which produces tamponade. (b) Sagittal reformatted contrast-enhanced CT image shows the pericardial defect (white arrowheads) and the herniating bowel loop with air (white arrow) compressing the anterior aspect of the heart (black arrowheads). Note the free edge of the diaphragm (black arrow). Pericardiocentesis demonstrated fecal material. The patient was taken to the operating room for repair of the hernia and resection of necrotic bowel found within the pericardial sac.
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Figure 21b. Pericardial tamponade in a 63-year-old woman with a delayed posttraumatic diaphragmatic hernia. (a) Contrast-enhanced CT image obtained at the level of the ventricles shows intrapericardial herniation of the colon (arrows), which produces tamponade. (b) Sagittal reformatted contrast-enhanced CT image shows the pericardial defect (white arrowheads) and the herniating bowel loop with air (white arrow) compressing the anterior aspect of the heart (black arrowheads). Note the free edge of the diaphragm (black arrow). Pericardiocentesis demonstrated fecal material. The patient was taken to the operating room for repair of the hernia and resection of necrotic bowel found within the pericardial sac.
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CT assessment of structures adjacent to the heart including mediastinal structures and the lungs may suggest the nature of pericardial effusion with or without tamponade. Pericardiac mediastinal structures that are well assessed at CT include the aorta and great vessels, esophagus, and thymus. Lung cancer can result in tamponade via metastatic pericardial or cardiac involvement (60). Aortic pathologic conditions that can result in tamponade include aortic dissection and aneurysm rupture (34,61,62) (Fig 22). Mediastinal pathologic conditions that can cause tamponade include mediastinal malignancy producing direct cardiac compression, such as lymphoma or small cell lung cancer. Examples of esophageal pathologic conditions that may produce tamponade include esophageal malignancy (63) and esophageal perforation (64). Other reported causes of tamponade that have been described at CT include abscess formation (Fig 23).
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Figure 22a. Type A aortic dissection with cardiac tamponade in a 74-year-old woman. (a) Contrast-enhanced multisection CT image shows a dilated ascending aorta that contains an intimal flap (arrowhead). (b) Axial CT image shows a pericardial effusion (arrows) and compression of the right ventricle.
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Figure 22b. Type A aortic dissection with cardiac tamponade in a 74-year-old woman. (a) Contrast-enhanced multisection CT image shows a dilated ascending aorta that contains an intimal flap (arrowhead). (b) Axial CT image shows a pericardial effusion (arrows) and compression of the right ventricle.
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Figure 23. Cardiac tamponade due to an abscess in a patient with a history of a gunshot wound. An intrapericardial purulent collection developed with regional cardiac tamponade due to compression of the left ventricle. CT image shows an intrapericardial abscess as a low-attenuation collection surrounded by enhancing pericardium (arrowhead).
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MR Imaging
MR imaging allows detection of pericardial effusions with high sensitivity, demonstrating fluid collections as small as 30 mL (8). However, MR imaging has a limited role in the setting of cardiac tamponade owing to the emergent and life-threatening nature of this condition. Nevertheless, there are isolated reports of imminent cardiac tamponade and cardiac rupture documented at MR imaging as an incidental finding (65,66). Some of the previously described findings with other imaging modalities can be seen with MR imaging, including the swinging heart (65) and paradoxical septal bounce, which can be easily seen on short-or long-axis cine MR images (6).
MR imaging can provide information useful in characterizing the nature of the pericardial effusion in addition to the effects on cardiac functioning and diastolic filling. Simple transudative effusions usually exhibit low signal intensity on T1-weighted or proton density–weighted spin-echo or double inversion images and high signal intensity on T2-weighted spin-echo, fast spin-echo, gradient-echo, or triple inversion images as well as steady-state free precession and fast cine images. The presence of septations and debris suggests a complex effusion. Hemorrhagic and proteinaceous or exudative effusions generally exhibit high signal intensity on T1- and T2-weighted images owing to the high protein content. Hemorrhage in the pericardial space usually exhibits low signal intensity on gradient-echo images; however, its appearance changes with time due to the degradation of blood products. The signal intensity characteristics with other sequences depend on the age and composition of the hemorrhagic effusion (4,6).
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Treatment
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Treatment of tamponade is drainage of the pericardial contents, preferably by using needle pericardiocentesis with echocardiographic, fluoroscopic, or CT guidance. However, therapeutic emergency pericardiocentesis without image guidance should be performed in cases of sudden circulatory collapse or hemodynamic instability (3).
The success rate of echocardiography-guided pericardiocentesis is 93% in patients with anterior effusions larger than 10 mm and only 58% in those with small, posteriorly located effusions. The success rate of echocardiography-guided pericardiocentesis in loculated pericardial effusions is 96% (67). Rescue echocardiography-guided pericardiocentesis relieved tamponade after cardiac perforation in 99% of a series of 88 patients and was the definitive therapy in 82% (68).
Fluoroscopy-guided pericardiocentesis and hemodynamic monitoring have a success rate of 93.1%, in comparison to emergency pericardiocentesis without image guidance, which has a success rate of only 73.3% (67).
Klein et al (69) reviewed 319 CT-guided pericardiocentesis procedures and reported a technical success rate of 98.4%; symptomatic improvement was documented in 79% of patients with tamponade and in 78% of patients with marked shortness of breath without other evidence of tamponade.
Surgical drainage is desirable in patients with intrapericardial bleeding, purulent effusion, or clotted hemopericardium. Patients with recurrent tamponade (ie, malignant tamponade) may require pericardial sclerosis or a balloon pericardiotomy to create a communication between the pericardium and the pleura or peritoneum (3).
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Conclusions
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Cardiac tamponade is a syndrome characterized by increased intrapericardiac pressure that leads to poor cardiac diastolic filling and decreased cardiac output. The radiologist should be aware of the pathophysiologic events and their corresponding imaging correlates in order to identify patients with this life-threatening condition, which requires prompt intervention. Although echocardiography remains the first-line imaging study in evaluation of pericardial effusion and suspected tamponade, CT can be a useful problem solving technique in patients with inconclusive echocardiographic findings. CT evaluation of the heart, pericardium, and surrounding structures can provide valuable information about the cause of this condition.
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Footnotes
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Abbreviations: IVC = inferior vena cava
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References
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