REVIEW ARTICLE

A Systematic Approach to Evaluation of Pericardial Effusion and Cardiac Tamponade

John R. Schairer, DO, Santanu Biswas, MD, Steven J. Keteyian, PhD, and Karthikeyan Ananthasubramaniam, MD
increase and decrease with respiration. The uctuations in volume are greater in the RV than in the LV because the RV wall is thinner than the LV wall. Under normal conditions, ow across the cardiac valves vary based on the phase of respiration: 10% to 15% across the mitral valve, 20% to 25% across the tricuspid valve, and 10% across the aortic and pulmonary valves.1,2,4

Abstract: Pericardial disease leading to pericardial effusion (PEF) is a common condition encountered by the clinician in day-to-day practice. If the PEF becomes large enough, it can cause hemodynamic compromise, resulting in a cardiogenic shock state known as cardiac tamponade. There are many clinical and echocardiographic signs that a clinician can use to assess whether a large PEF is hemodynamically signicant. However, these signs can be either conicting or even absent. The purpose of this review is to rst, describe the physiology of the pericardium in health and how it changes with disease; second, outline the pathophysiology of pericardial tamponade and discuss how it is responsible for the physical and echocardiographic ndings of cardiac tamponade; and third, suggest an approach to applying these ndings in a systematic order to ensure a correct diagnosis. Key Words: pericardial disease, tamponade, pericardial effusion, cardiogenic shock (Cardiology in Review 2011;19: 233238)

PATHOPHYSIOLOGY OF PEF AND CT

The pericardium is composed of a parietal and a visceral layer.1,2,57 The visceral layer of the pericardium, when inamed, forms an increased amount of PEF. As the PEF increases in size, it increases the pressure in the pericardial space. In situations of gradual accumulation of PEF, as in malignancy and chronic kidney disease, PEF can become quite large without signs of CT. When PEF accumulates rapidly, as can occur with perforation of a chamber wall or postcardiotomy hematomas in the pericardial space, the inelastic property of the pericardium prevents stretching and causes the pressure in the pericardial space to increase rapidly. This can lead to CT even with small amounts of PEF. The hemodynamic consequences of increased pericardial pressure are initially diastolic dysfunction, with limitation of cardiac lling that ultimately becomes cardiogenic shock with compression of the cardiac chambers to the point cardiac output decreases and systolic blood pressure falls. In CT, the ventricles are no longer lling against the diastolic pressures of the individual chamber, but rather against the common pressure of the intrapericardial space. Also, the total intrapericardial volume, consisting of pericardial uid and heart volume, is xed. The lling of each ventricle depends on the competing left and right diastolic pressures that are generated by the pulmonary and systemic venous beds, respectively.8 The changes in reciprocal ow that normally occur during respiration, between the right and left side of the heart, are exaggerated. The exaggerated shifting of the septum during respiration is in the direction of the smaller ventricle.9 This phenomenon is known as ventricular interdependence.1 Ventricular interdependence is the physiologic mechanism to explain the exaggerated respiratory variation in Doppler ows across all 4 cardiac valves and exaggerated respiratory variation in systolic blood pressure known as pulsus paradoxus (PP).10 13 Reddy et al,8,14 describe the hemodynamics of patients with PEF and CT. They measured hemodynamic parameters before, during, and after pericardiocentesis. Baseline hemodynamics revealed equalization of the right atrial (RA), intrapericardial, and wedge pressures at 16 mm Hg. PP was also observed. The authors then divided the hemodynamics of CT into 3 phases of increasing hemodynamic compromise, beginning with a PEF with little hemodynamic effect (ie, phase 1) and culminating in CT and cardiogenic shock (ie, phase 3) (Fig. 1). Because the hemodynamics of CT develop over 3 phases, CT should be viewed not as an all or none clinical state, but as a clinical condition that is part of a continuum. Additional important ndings in their study were as follows: (1) RA pressure is always equal to or higher than pericardial pressure; (2) if pericardial pressure is less than the LV diastolic pressure, then cardiac output is still normal, although slightly www.cardiologyinreview.com | 233

ericardial disease leading to pericardial effusion (PEF) is a common condition encountered by the clinician in day-to-day practice. If the PEF becomes large enough it can cause hemodynamic compromise, resulting in a clinical condition known as cardiac tamponade (CT). There are many clinical and echocardiographic signs that a clinician can use to assess whether a large PEF is hemodynamically signicant (Table 1). However, these signs are often either conicting or sometimes even absent. The purpose of this review is to rst, describe the physiology of the pericardium in health and how it changes with disease; second, outline the pathophysiology of CT and associated physical and echocardiographic ndings of CT; and third, suggest a systematic approach to applying these ndings to ensure a correct diagnosis.

NORMAL PHYSIOLOGY OF THE PERICARDIUM

Normally, the intrapericardial and intrathoracic pressures are equal and vary between 5 and 5 mm Hg during expiration and inspiration, respectively.13 The low pressure in the pericardial space allows the respiratory variation in intrathoracic pressure to be reected in the intracardiac pressures. With inspiration, intrathoracic pressure decreases, causing an increased ow into the right side of the heart. With inspiration, there is also a decrease in the gradient between the pulmonary veins and the left atrium (LA), causing decreased ow into the left side of the heart. During expiration the process is reversed. As a result, right ventricle (RV) and left ventricle (LV) size, as well as right- and left-sided stroke volume,

From the Department of Internal Medicine, Heart and Vascular Institute, Henry Ford Hospital, Detroit, MI. The authors declare no conict of interest. Correspondence: John R. Schairer, DO, Department of Medicine, Heart and Vascular Institute, Henry Ford Hospital, K-14, Detroit, MI 48202. E-mail: jschair1@hfhs.org. Copyright 2011 by Lippincott Williams & Wilkins ISSN: 1061-5377/11/1905-0233 DOI: 10.1097/CRD.0b013e31821e202c

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TABLE 1. Physical and Echocardiographic Doppler Signs Indicating Pericardial Effusion and/or Tamponade
Pulsus paradoxus Loss of the Y descent on the jugular venous pulse Pericardial effusion on echocardiograph RV collapse RA collapse IVC plethora (dilated IVC with lack of inspiratory collapse) Increased respiratory variation of ow across the mitral, aortic, and tricuspid valves Ventricular interdependence (shifting of the septum in response to respiration with variation in ventricular dimensions) Swinging heart LA or LV collapse (rare)
RV indicates right ventricular; RA, right atrial; IVC, inferior vena cava; LA, left atrial; LV, left ventricular.

the normal apical impulse position compared with increased cardiac borders on percussion, auscultatory dullness along left scapular area, and enlarged radiographic cardiac silhouette.

Phase 2: Pretamponade
During phase 2, the intrapericardial and RA pressures continue to increase until they equal the LA pressure at the end of phase 2 and the beginning of phase 3. Increased intrapericardial pressure causes cardiac chambers to decrease in size and secondarily cardiac output to decrease, but there are no signs of shock. Many of the echocardiographic signs of CT will begin to become apparent during phase 2, although classically they are found in phase 3. There is a further decrease in arterial pressure during inspiration, approaching the 10 mm Hg, consistent with PP. Recognizing phase 2 CT is important because it allows one to predict impending CT and intervene before the patient goes into shock, something that can happen very quickly.

Phase 3: CT
Phase 3 begins with equalization of intrapericardial, RA, and LA pressures. During this phase, there are further increases in the pressures with a further drop in cardiac output; the fall in systolic pressure during inspiration is now 10 mm Hg and circulatory collapse occurs. Cardiogenic shock or CT ensues. PP is the sine quo non of phase 3 CT. Originally described by Kussmaul in 3 patients with large PEF,15 PP is an exaggeration of a normal inspiratory drop of systolic pressure, usually 10 mm Hg. Although PP was originally thought to occur only if there was equalization of pressures (ie, phase 3), a few patients will demonstrate this nding during phase 2. Finally, it is important to recognize that PP may not always be present in CT16 and that it can be seen in other disease processes also (Table 2).12,1721

FIGURE 1. Pathophysiology of cardiac tamponade. Phase 1: intrapericardial pressure RA pressure LV filling pressure. Phase 2: begins with equalization of intrapericardial and RA pressures. Phase 3: begins with equalization of intrapericardial, RA and LV filling pressures. RA indicates right atrium; LV, left ventricle. depressed; (3) the inspiratory fall in systolic blood pressure is more than normal but may not always meet criteria for PP; (4) when RV lling pressure rises and equals LV lling pressure, the hemodynamic changes of CT result and PP is present; and (5) pulmonary artery wedge pressure, which reects LV diastolic pressure, is elevated and it will be transiently greater and less than pericardial pressure during inspiration and expiration. The latter contributes to the changes in cardiac ow with respiration and is the mechanism responsible for PP.

ECHOCARDIOGRAPHY AND DOPPLER IN PEF AND CT Echocardiographic Evaluation of PEF

Echocardiography is the cornerstone of initial imaging in the diagnosis of PEF and its complications. A major role of echocardiography is in determining the size and location of the PEF. PEF size is designated physiologic (2550 mL) if there is no separation of

TABLE 2. Comorbid Conditions Affecting Pulsus Paradoxus

Conditions in which pulsus paradoxus may be present without pericardial tamponade Obesity Asthma; chronic obstructive pulmonary disease Right ventricular infarction Pulmonary embolism Effusive-constrictive pericardial tamponade Heart failure Constrictive (rare) Conditions in which pulsus paradoxus may be absent with pericardial tamponade16 Aortic regurgitation Atrial septal defect Right ventricular hypertrophy without pulmonary hypertension Cardiogenic shock with severe pericardial tamponade Increased left ventricular lling pressures and diastolic stiffness Local pericardial adhesions Positive pressure breathing

CLINICAL FINDINGS IN PEF AND CT Phase 1: The Early Phase of Pericardial Fluid Accumulation
During phase 1, the increase in uid in the pericardial space causes a gradual increase in the intrapericardial pressure that results in an increase in both RV and LV lling pressures. At the end of phase 1, RV lling pressure and the intrapericardial pressure are equal at approximately 10 mm Hg, and there is a small decrease in cardiac output and arterial pressure during inspiration, but it is still within the range of normal. The LV lling pressure is still slightly higher than the pericardial pressure (Fig. 1). The main clinical ndings of phase 1 are due to the large size of the PEF. Some important clinical clues at this stage could be discrepancy between 234 | www.cardiologyinreview.com

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the pericardium and epicardium during diastole, small ( 100 mL) if the echocardiographic-free space in systole and diastole is 10 mm, moderate (100 500 mL) if the echocardiographic-free space is between 10 and 20 mm, and large ( 500 mL) if the echocardiographic-free space is 20 mm.1,5,2224 An alternate method of describing the size of the PEF takes into account that the PEF is not uniformly distributed around the heart and recommends making several measurements around the circumference of the pericardium, annotating their location so that on repeat studies it can more accurately be determined if the effusion is changing size. A swinging heart on the echocardiograph is a sign of a large PEF and possibly CT. The rst hemodynamic change to occur with an enlarging PEF is an increase in RA pressure manifested clinically as jugular venous distention or echocardiographically as inferior vena cava (IVC) dilatation. The diameter of the IVC and its change with respiration are easily visualized echocardiographically with subcostal views.4 The American Society of Echocardiography25 has recently published an update on the estimation of RA pressures (Table 3). Beginning with phase 1 where IVC caliber and collapsibility are normal, there is progressive dilatation of IVC and decrease in collapsibility with respiration in phase 2. When RA pressures exceed 15 mm Hg, there is signicant dilation of IVC with minimal or no variation in size with respiration (IVC plethora).26 28 If IVC plethora is present, the sniff test should be performed to conrm that the IVC pressures are truly elevated. The sensitivity of IVC plethora for CT is 97% while the specicity is somewhat lower at 66% (Table 4). Without IVC plethora, it is unlikely the patient has cardiac CT.

velocity increased by 85% and 58%, respectively, with inspiration. In general, variations in E wave velocities during respiration across the mitral valve, tricuspid valve, and pulmonary outow that are greater than 25%, 50%, and 30%, respectively, indicate CT. Similar changes can be seen during the respiratory cycle for the isovolumic relaxation time, left ventricular ejection time, and the time velocity index across all valves as well as in the descending aorta. The pathophysiology for the exaggerated changes seen during the respiratory cycle is the same as for PP. When evaluating respiratory changes in PEF and suspected CT, other disease states that may demonstrate an increase in respiratory ow variation across the valves should be eliminated or accounted for. These include chronic obstructive lung disease, pericardial constriction, severe tricuspid regurgitation, and RV dysfunction. One of the major differences between respiratory variation seen in CT versus other conditions is that the maximal change in the peak E-wave velocity during inspiration will happen in the very rst beat after inspiration in CT as compared with a more gradual drop in E-wave velocity with conditions such as chronic obstructive pulmonary disease or asthma.30

Echocardiographic Evaluation of CT
Because of the increased pressure in the pericardial space in CT, there is a reduction in size of the RV chamber, collapse of the RV during ventricular diastole, or RA inversion during atrial diastole.31 40 RV collapse occurs during diastole because the pericardial pressure exceeds the RV early diastolic pressure (Fig. 2). Armstrong et al32 retrospectively applied the nding of RV diastolic collapse to 91 patients with moderate to large PEF. Using M-mode echocardiography, they showed that RV chamber size achieved its smallest dimension after the onset of the E wave of the mitral valve and after the closure of the aortic valve (ie, during diastole), when the RV should be dilating in response to passive lling. RV diastolic collapse was present in 16 of 17 patients with clinical CT. It involved the free wall of the RV outow tract and is most easily identied in the parasternal long axis or subcostal views, where the timing of the opening of the mitral valve and passive lling of the RV can be visualized simultaneously. It was also present in 7 of 69 patients who did not have clinical CT, but did have moderate to large PEFs, suggesting that RV collapse may be a very early sign of CT or that these patients are transitioning between phase 2 and phase 3. In all cases, the abnormal motion reverted back to normal after drainage of the PEF. Because of the RV collapse in early diastole, the lling of the RV now depends almost exclusively on atrial contraction and is another mechanism responsible for the decrease in cardiac output during CT. Hemodynamically, this is manifested by loss of the Y-descent of the V wave while the X-descent of the A wave of the RA waveform is preserved. Leimgruber et al41 reported that RV

Doppler Evaluation in CT
Appleton et al29 described the changes in E-wave velocity with respiration across the mitral and tricuspid valves in normal patients, patients with large PEF, and those with CT. The percentage change of E-wave velocity was determined as INSP EXP/EXP, where INSP is the rst beat of inspiration and EXP is the rst beat of expiration. With CT, mitral valve E-wave velocity and A-wave velocity decreased by 43% and 25%, respectively, during inspiration. In contrast, the tricuspid valve E-wave velocity and A-wave

TABLE 3. Estimation of Right Atrial Pressure Using Inferior Vena Cava25

Inferior Vena Cava Diameter Normal ( Dilated ( Dilated ( Dilated ( 2.1 cm) 2.1 cm) 2.1 cm) 2.1 cm) Change in Diameter With Respiration or Sniff Test Decrease Decrease Decrease Decrease 50% 50% 50% 50% Estimated Right Atrial Pressure 3 mm Hg (range: 05) 8 mm Hg (range: 510) 8 mm Hg (range: 510) 15 mm Hg

TABLE 4. Sensitivity and Specificity of Signs for Pericardial Tamponade in Patients With Large Pericardial Effusion
Sensitivity RA collapse RA collapse 1/3 cardiac cycle RV collapse IVC plethora Large PEF 55% 94% 48% 97% 73% Specicity 88% 100% 95% 66% 97% PPV 10% 38% 7% 45% NPV 99% 99% 99% 99%

RA indicates right atrium; RV, right ventricle; IVC, inferior vena cava; PEF, pleural effusion; PPV, positive predictive value; NPV, negative predictive value.

FIGURE 2. Pathophysiology of right ventricle (RV) and right atrial (RA) collapse. Pericardial pressure exceeds RV and RA pressure causing collapse. www.cardiologyinreview.com | 235

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collapse was associated with a 21% decrease in cardiac output. Furthermore, RV diastolic collapse seems to better predict the abnormal hemodynamics of CT than PP. RA collapse or inversion was rst described by Gillam et al33 (Fig. 2). They studied 127 patients with moderate or large PEF; 19 patients were thought to have CT. In addition, they calculated the percentage of the cardiac cycle which RA inversion occupied and referred to it as the RA inversion time index. Seventeen of the 18 patients with CT and interpretable data had RA inversion time index 0.34 yielding 94% sensitivity. Eighteen patients who had demonstrated RA inversion, but did not have CT had a RA inversion time index 0.34 yielding a specicity of 100%, a predictive value of 100%, and an accuracy of 97%. The RA inversion time index is believed to be the most sensitive nding for CT. The absence of sinus rhythm does not preclude the use of RA collapse to make the diagnosis of CT. False-negative and false-positive ndings occur for both RA inversion and RV collapse. False negatives occur in patients with elevated right heart pressures or RV hypertrophy, both of which counter the increased pericardial pressures. One cause of RV diastolic collapse that is unrelated to CT is a large pleural effusion. Table 4 compares the sensitivity and specicity of the common echocardiographic signs of CT.

had 1 of these end points. By univariate analysis, each sign was associated with CT or the combined end point. When data were analyzed with logistic regression modeling, PEF size was the most powerful predictor of outcome (CT: odds ratio 51, 95% condence interval 3.5729, P 0.004; combined end point CT, pericardiocentesis, and/or surgical drainage : odds ratio 78, 95% condence interval 14 421, P 0.0001).

CT IN THE ABSENCE OF SUPPORTIVE FINDINGS

If a patient has a large PEF and CT is suspected, evaluating the patient for comorbid conditions that may cause false-positive or false-negative ndings is an important rst step. For example, patients with pulmonary hypertension and RV hypertrophy may not manifest the sign of right heart collapse until later in the course of CT. Clinical scenarios in which the usual signs of CT will be affected by the comorbid condition are discussed later in the proceeding paragraphs.

Hydration
Klopfenstein et al45 and Cogswell et al46 studied in an experimental model how alterations in intravascular volume affected right heart chamber collapse and hemodynamic severity of CT. In hypovolemia, RV collapse occurred at a lower intrapericardial pressure, aortic blood pressure, and cardiac output. Conversely, volume expansion resulted in RV collapse occurring at higher intrapericardial pressures. When compared with PP, the 2 tests were equally sensitive in the hypovolemic state, but RV collapse was more sensitive in the euvolemic and hypervolemic state.

Prognostic Implication of Echocardiographic Diagnosis of CT: Detection Before Hemodynamic Embarrassment

Findings of CT, such as RA and RV collapse, increased respiratory variation, and PP, can begin during phase 2; a time when pericardial pressure is increased but there is no hemodynamic collapse.31,41,42 For example, Appleton et al29 reported that some patients with a large PEF could have a variation in ow velocity that exceeds normal values, but is not enough to meet the criteria for CT. With pericardiocentesis, these ow velocities returned to normal, suggesting a pretamponade state. Just as CT is not an all or none pathologic process, the echocardiographic signs of CT should not be viewed as present or absent, but as a continuum to follow the course of CT. In a hemodynamically stable patient, the development of an 8 mm Hg PP or a respiratory variation across the mitral valve of only 20% may signal impending CT, allowing one to intervene before the patient goes into shock. Eisenberg and Schiller43 applied the concept of Bayes Theorem to the diagnosis of CT by reviewing 8 articles that reported the sensitivity and specicity for RA and RV collapse and IVC plethora and applied them to the positive and negative predictive values for populations with different pretest probabilities of CT. Using reported intermediate sensitivities and specicities in a patient population with a 50% pretest probability of having CT would then yield a positive predictive value of 90% and a negative predictive value of 20%, with a false-positive rate of 14% to 22% and a false-negative rate of 11% to 12%. In contrast, in a low-risk population with a pretest probability 10%, the incidence of false-positive tests is in the range of 92% to 98%, whereas the negative predictive value of these tests is 99%. Thus, pretest probability of CT could help to show how one interprets the echocardiographic signs of a PEF. In a patient with a small PEF, the absence of the signs of CT is very helpful, but their presence is less so. This is in contrast to the patient with a large PEF in whom the signs of CT have a high positive predictive value and low negative predictive value. In a follow-up article, the same authors addressed the prognostic value of echocardiography in 187 hospitalized patients with PEF.44 They found that 6% of the PEF were large, 21% were moderate, and 73% were small. Nine patients (5%) had CT, 11 (6%) had pericardiocentesis, 8 (4%) had surgical drainage, and 16 (9%) 236 | www.cardiologyinreview.com

Mechanical Ventilation
An important and commonly encountered scenario of altered physiology obscuring the signs of CT is noted in the patient on a mechanical ventilator. The clinical and echocardiographic signs one looks for to indicate CT are either absent or opposite of what one would expect.1,47,48 Specically, intrathoracic pressure during inspiration instead of being negative is now positive and more positive than during expiration. Doppler recording of ow across the tricuspid valve is now greater in expiration, and ow across the mitral is greater with inspiration, and both ow velocity changes with respiration are attenuated. PP and the exaggerated respiratory variation across the mitral and tricuspid valves usually seen in CT are absent. Also, if the patient is on the ventilator because of lung disease, they may have pulmonary hypertension and/or RV hypertrophy and may not demonstrate RA or RV collapse even in the presence of CT.

Low-Pressure CT
Low-pressure CT is a clinical condition in which a large PEF associated with low intrapericardial pressure results in circulatory collapse. It was rst described in 1979 by Antman et al49 In 2006, Sagrista-Sauleda et al50 reported their 19-year experience during which 29 patients met their criteria for low-pressure CT; dened as an intrapericardial pressure 7 mm Hg during CT and a RA pressure 4 mm Hg after the intrapericardial pressure had been lowered to 0 mm Hg with pericardiocentesis. Only 24% of patients with low-pressure CT versus 71% of patients with classic CT demonstrated the usual clinical ndings (ie, PP, jugular venous distention). Although initially thought to be secondary to hypovolemia, Sagrista-Sauleda et al50 also found clinical evidence of hypovolemia in only a minority of patients, and the patients in his study recovered uneventfully after pericardiocentesis without uid replacement therapy.

Elevated Left Ventricular Filling Pressure

For PP to occur, both chambers must be lled against a common pressure (ie, the pericardial pressure, and the RV and LV 2011 Lippincott Williams & Wilkins

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lling pressures must be equal).14,51 In patients with a signicant increase in LV lling pressure due to hypertension or uremia, RV lling pressure and pericardial pressure must rise to even higher levels than usual to equilibrate with the LV pressure. Hemodynamic collapse can develop without the signs of CT being present.

Miscellaneous Conditions
Loculation of the PEF over a chamber or chambers of the heart because of localized pericardial adhesions can cause regional CT, and in this instance localized chamber collapse may be noted. For example, if the PEF is limited to the LV, LV collapse can be seen. Because the lling pressures of the 2 ventricles are unequal, PP is absent. Regional CT usually occurs in patients who have recently undergone cardiac surgery. In aortic regurgitation, the LV is partially lled by the regurgitant volume; therefore, the respiratory variation in LV lling becomes less important. Similarly, in patients with atrial septal defects, the left and right atria act as a single atrium, nullifying the changes in lling that occur in response to changes in intrathoracic pressures.1,5256 Many of the signs of CT may not present in these conditions.

erate to large PEF is the most powerful indicator of outcomes. Third, while the sensitivities and specicities of the signs for CT are high, their predictive values are dependent on the pretest likelihood of disease (ie, the size of the PEF). The next step is to estimate RA pressure (Table 3). If the RA pressure is 10 mm Hg, the patient is probably in phase 2 CT. IVC plethora corresponds to RA pressure 15 mm Hg and the patient is probably in phase 3 CT, assuming there are no other causes for an elevated RA pressure. RA inversion for greater than one-third of the systole and RV diastolic collapse, PP, and exaggerated respiratory variation across the mitral and tricuspid valves serve as conrming signs of CT. The patients with clinical signs of CT but no echocardiographic criteria for CT (ie, respiratory variation across the mitral and tricuspid valves 25% and 50%, respectively, systolic fall in the blood pressure with inspiration of 10 mm Hg, borderline RV and RA collapse) could be in phase 2 or impending CT. They require close monitoring. Evaluation of conditions that interfere with echocardiographic signs of CT as discussed previously should be evaluated. Finally, if a patient with a moderate to large PEF is demonstrating circulatory collapse, one must consider CT as the cause and consider pericardiocentesis even if the signs for CT are not conclusive.

USE OF COMPUTED TOMOGRAPHY AND MAGNETIC RESONANCE IMAGING IN THE EVALUATION OF CT

Echocardiography remains the primary imaging modality for evaluating the presence and hemodynamic signicance of PEF primarily due to its portability, rapid image acquisition and interpretation, and more robust hemodynamic evaluation; however, computed tomography and magnetic resonance imaging offer complementary advantages due to the larger eld of view, higher contrast resolution, and better tissue characterization. Although computed tomography is very sensitive in detecting PEFs, it tends to overestimate the volume of PEF.57,58 A recent study showed that echocardiography correlated better to the amount of uid drained at pericardiocentesis than computed tomography.59 In patients with CT, a number of correlative hemodynamic ndings have been observed, such as RV wall collapse, the swinging cardiac motion in the pericardial space, IVC and superior vena cava dilation, periportal lymphedema, coronary sinus compression, and reux of contrast medium into the azygous vein.60 66 However, these signs have only been reported in case reports or very small studies; thus, the full value of these signs in predicting CT remains investigational. The entire chest was visualized so that mediastinal masses, enlarged lymph nodes, and aortic dissection could be excluded. The enhanced eld of view allows for easy differentiation between pericardial and pleural effusions as well as enhanced sensitivity for loculated PEFs. Computed tomography and magnetic resonance imaging allows for better characterization of the effusion itself, and so, the differentiation of hemorrhagic malignant effusions from simple effusions is possible. Finally, pericardial thickness, an important nding in the diagnosis of pericardial disease, is more reliably measured with computed tomography or magnetic resonance imaging than with echocardiography.

ACKNOWLEDGMENTS
The authors thank Nandita S. Mani and Clinton A. Brawner for their contribution in preparing and submitting the manuscript. REFERENCES
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SYSTEMATIC APPROACH TO THE APPLICATION OF THE CLINICAL AND ECHOCARDIOGRAPHIC FINDINGS TO DIAGNOSE CT
As a rst step, the patient needs to be evaluated for signs of clinical instability, that is, sinus tachycardia, a drop in blood pressure by 20 mm Hg, or blood pressure 100 mm Hg. Second, it is important to determine the size of the PEF and make several measurements, documenting their location. The presence of a mod 2011 Lippincott Williams & Wilkins

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