Echocardiography in Pericardial Disease Samuel Wann, MD, FASE, and Edward Passen, MD, Milwaukee, Wisconsin; and Chicago, Illinois Since its introduction into clinical cardiology in the 1960’s, echocardiography has become an essential and integral part of the evaluation of the cardiac patient. Dr. Harvey Feigenbaum had a seminal role in popularizing echocardiography. Detection of pericardial effusion was one of the first applications of echocardiography to gain widespread acceptance. Over the past 40 years, echocardiography has become a ubiquitous, first line tool for evaluating the pericardium and other cardiac structures. Keywords: Echocardiography, Pericardium, Cardiac tamponade, Cardiac constriction By his own account, Harvey Feigenbaum 1 was not the first to describe the use of reflected ultrasound to detect pericardial effusion. Inge Edler, 2 an early pioneer in the use of high-frequency sound waves for cardiac diagnosis, published the first ultrasound images of an anterior pericardial effusion in 1961. 3 Other investigators also described the use of cardiac ultrasound to detect pericardial fluid, 4-7 but Dr Feigen- baum 8 was clearly one of the first to recognize the enormous clinical potential of ultrasound for detecting pericardial effusion. His early studies using A-mode (Figure 1), M-mode, and later two-dimensional echocardiography, as well as his vision and passion, were instrumen- tal in promoting the widespread use of echocardiography, a term he helped popularize, as a practical tool for accurate, noninvasive detec- tion of pericardial effusion. 8-12 These early observations also intro- duced clinicians everywhere in the broader potential of echocardiog- raphy at a time when the diagnosis of mitral stenosis was its primary but limited role. Before the introduction of echocardiography, detection of pericar- dial effusion was often a difficult diagnostic challenge, sometimes requiring potentially hazardous procedures, such as cardiac catheter- ization or even blind pericardiocentesis, to confirm a clinical sugges- tion. Although the history, physical examination, electrocardiogram, and chest radiograph are useful in the investigation of pericardial disease, all lack the sensitivity and specificity of the echocardiogram. Introduction of the echocardiogram revolutionized the evaluation of pericardial disease and echocardiography continues to be the primary diagnostic tool for assessing the spatial distribution and functional significance of pericardial diseases. As shown in Figure 2, the pericardium surrounds the heart and extends to insert on the proximal great vessels. The pericardium consists of a visceral layer, which is contiguous with the epicardium of the heart, and a parietal layer, which forms a sac around the heart. The phylogenetic purpose of the pericardium is unclear. 13,14 Ana- tomically, the pericardium isolates the heart from the rest of the mediastinum and thorax. Physiologically, the pericardium may have little if any significant role under normal circumstances, but it is affected by a variety of disease conditions often with major clinical consequences. 15 Echocardiography can be useful in detecting a variety of conditions that affect the pericardium including: (1) partial or complete absence of the pericardium; (2) primary pericardial cysts and both primary and metastatic pericardial tumors; (3) inflammation with secondary effusion as a result of bacterial or viral infection, myocardial infarction, trauma, uremia, neoplasm, hypothyroidism, or high-dose radiation exposure; (4) pericardial tamponade that occurs when the fluid accumulation causes an increase in pressure in the pericardial sac, pressing on the heart and interfering with normal filling/function; and (5) pericardial constriction as a result of thickening, fibrosis, and adherence between the layers of the pericardium, constricting the heart, and impairing diastolic filling. PERICARDIAL EFFUSION Echocardiography is usually the primary diagnostic method used for initial detection of pericardial effusion. As shown in Figure 3, pericar- dial fluid is recognized as an echo-free space between the visceral and parietal pericardium surrounding the heart. Pericardial fluid first accumulates posterior to the heart, when the patient is examined in the supine position, as the heart itself usually floats in transudative pericardial fluid. Small pericardial effusions are generally visualized as small echo-free spaces in the posterior atrioventricular groove, and small amounts of fluid can be present even in healthy individuals. As the effusion increases, it extends laterally and with large effusions the echo-free space expands to surround the entire heart. Large effusion also extends behind the left atrium (between the posterior atrial wall and the aorta) (Figure 4) and can, thus, be differentiated from pleural effusions, which do not usually appear immediately posterior to the left atrium. Two-dimensional echocardiography is generally quite sensitive and specific in detecting pericardial effusion (both free and loculated), and can be used to estimate the amount of fluid present. Very small pericardial effusions may be most obvious during systole. An echo- free space appearing only anterior to the heart is usually caused by pericardial fat, not effusion (Figure 5). Differentiating pericardial fat from localized pericardial effusion can be difficult in some patients. Computed tomography may be helpful. 16 It is difficult to characterize the origin of fluid in the pericardial space by its echocardiographic appearance alone, but hemorrhagic or purulent fluid (Figure 6) may be more echogenic than simple serous fluid. Fibrinous bands and mass lesions can sometimes be seen in the From the Wisconsin Heart Hospital, Milwaukee, Wisconsin (S.W.), and Advocate Lutheran General Hospital, Chicago, Illinois (E.P.). Reprint requests: Samuel Wann, MD, Wisconsin Heart Hospital, 10000 Blue- mound Rd, Milwaukee, WI 53226 (E-mail: [email protected]). 0894-7317/$34.00 Copyright 2008 by the American Society of Echocardiography. doi:10.1016/j.echo.2007.11.003 7
Transcript
doi:10.1016/j.e
Echocardiography in Pericardial DiseaseSamuel Wann, MD, FASE, and Edward Passen, MD, Milwaukee, Wisconsin; and Chicago, Illinois
Since its introduction into clinical cardiology in the 1960’s, echocardiography has become an essential andintegral part of the evaluation of the cardiac patient. Dr. Harvey Feigenbaum had a seminal role inpopularizing echocardiography. Detection of pericardial effusion was one of the first applications ofechocardiography to gain widespread acceptance. Over the past 40 years, echocardiography has becomea ubiquitous, first line tool for evaluating the pericardium and other cardiac structures.
By his own account, Harvey Feigenbaum1was not the first to describethe use of reflected ultrasound to detect pericardial effusion. IngeEdler,2 an early pioneer in the use of high-frequency sound waves forcardiac diagnosis, published the first ultrasound images of an anteriorpericardial effusion in 1961.3 Other investigators also described theuse of cardiac ultrasound to detect pericardial fluid,4-7 but Dr Feigen-baum8 was clearly one of the first to recognize the enormous clinicalpotential of ultrasound for detecting pericardial effusion. His earlystudies using A-mode (Figure 1), M-mode, and later two-dimensionalechocardiography, as well as his vision and passion, were instrumen-tal in promoting the widespread use of echocardiography, a term hehelped popularize, as a practical tool for accurate, noninvasive detec-tion of pericardial effusion.8-12 These early observations also intro-duced clinicians everywhere in the broader potential of echocardiog-raphy at a time when the diagnosis of mitral stenosis was its primarybut limited role.
Before the introduction of echocardiography, detection of pericar-dial effusion was often a difficult diagnostic challenge, sometimesrequiring potentially hazardous procedures, such as cardiac catheter-ization or even blind pericardiocentesis, to confirm a clinical sugges-tion. Although the history, physical examination, electrocardiogram,and chest radiograph are useful in the investigation of pericardialdisease, all lack the sensitivity and specificity of the echocardiogram.Introduction of the echocardiogram revolutionized the evaluation ofpericardial disease and echocardiography continues to be the primarydiagnostic tool for assessing the spatial distribution and functionalsignificance of pericardial diseases.
As shown in Figure 2, the pericardium surrounds the heart andextends to insert on the proximal great vessels. The pericardiumconsists of a visceral layer, which is contiguous with the epicardium ofthe heart, and a parietal layer, which forms a sac around the heart.The phylogenetic purpose of the pericardium is unclear.13,14 Ana-tomically, the pericardium isolates the heart from the rest of themediastinum and thorax. Physiologically, the pericardium may havelittle if any significant role under normal circumstances, but it is
From the Wisconsin Heart Hospital, Milwaukee, Wisconsin (S.W.), and AdvocateLutheran General Hospital, Chicago, Illinois (E.P.).
Reprint requests: Samuel Wann, MD, Wisconsin Heart Hospital, 10000 Blue-mound Rd, Milwaukee, WI 53226 (E-mail: [email protected]).
0894-7317/$34.00
Copyright 2008 by the American Society of Echocardiography.
cho.2007.11.003
affected by a variety of disease conditions often with major clinicalconsequences.15
Echocardiography can be useful in detecting a variety of conditionsthat affect the pericardium including: (1) partial or complete absenceof the pericardium; (2) primary pericardial cysts and both primaryand metastatic pericardial tumors; (3) inflammation with secondaryeffusion as a result of bacterial or viral infection, myocardial infarction,trauma, uremia, neoplasm, hypothyroidism, or high-dose radiationexposure; (4) pericardial tamponade that occurs when the fluidaccumulation causes an increase in pressure in the pericardial sac,pressing on the heart and interfering with normal filling/function; and(5) pericardial constriction as a result of thickening, fibrosis, andadherence between the layers of the pericardium, constricting theheart, and impairing diastolic filling.
PERICARDIAL EFFUSION
Echocardiography is usually the primary diagnostic method used forinitial detection of pericardial effusion. As shown in Figure 3, pericar-dial fluid is recognized as an echo-free space between the visceral andparietal pericardium surrounding the heart. Pericardial fluid firstaccumulates posterior to the heart, when the patient is examined inthe supine position, as the heart itself usually floats in transudativepericardial fluid. Small pericardial effusions are generally visualized assmall echo-free spaces in the posterior atrioventricular groove, andsmall amounts of fluid can be present even in healthy individuals. Asthe effusion increases, it extends laterally and with large effusions theecho-free space expands to surround the entire heart. Large effusionalso extends behind the left atrium (between the posterior atrial walland the aorta) (Figure 4) and can, thus, be differentiated from pleuraleffusions, which do not usually appear immediately posterior to theleft atrium.
Two-dimensional echocardiography is generally quite sensitiveand specific in detecting pericardial effusion (both free and loculated),and can be used to estimate the amount of fluid present. Very smallpericardial effusions may be most obvious during systole. An echo-free space appearing only anterior to the heart is usually caused bypericardial fat, not effusion (Figure 5). Differentiating pericardial fatfrom localized pericardial effusion can be difficult in some patients.Computed tomography may be helpful.16
It is difficult to characterize the origin of fluid in the pericardialspace by its echocardiographic appearance alone, but hemorrhagic orpurulent fluid (Figure 6) may be more echogenic than simple serous
fluid. Fibrinous bands and mass lesions can sometimes be seen in the
7
8 Wann and Passen Journal of the American Society of EchocardiographyJanuary 2008
pericardial space. Percutaneous needle pericardiocentesis may besafely performed under real-time echocardiography guidance17 (Fig-ure 7, A). Successful removal of the pericardial fluid can be readilydocumented (Figure 7, B and C).
CARDIAC TAMPONADE
The pericardial sac can gradually stretch to accommodate increasing
Figure 1 A-mode echocardiogram from Dr. Feigenbaum’s1965 publication8 recorded in a patient before (top panel) andafter (bottom panel) pericardiocentesis. “PW” was thought tobe the posterior wall of the left ventricle, separated from “P,”the pericardium-fluid interface, by a pericardial effusion. Thisseparation disappeared following pericardiocentesis. Similarfindings were demonstrated during intrapericardial saline injec-tion in 5 mongrel dogs.
Figure 2 CT “pericardiogram.” Iodinated contrast material wasinadvertently injected into the pericardial space during anattempted pulmonary angiogram. The catheter perforated thecoronary sinus. Note that the contrast in the pericardial spaceis seen not only around the ventricles and atria, but extends intothe pericardial reflection on the proximal pulmonary artery andaorta. Catheter based pulmonary angiography has largely beenabandoned in favor of CT pulmonary angiography with periph-eral venous injection of contrast.
volume, but at any point in time, the total intrapericardial volume is
relatively fixed throughout the cardiac cycle. When the ability of thepericardium to stretch is exceeded by rapid or massive accumulationof fluid, any additional fluid causes the pressure within the pericardialsac to increase. When the increasing intrapericardial pressure exceedsthe intracardiac pressure, the positive transmural pressure gradientcompresses the adjacent cardiac chamber or chambers. Becauseintracardiac pressures vary throughout the cardiac cycle, the pericar-dial pressure will exceed the intracardiac pressure within differentchambers at different points in the cardiac cycle. The chambers withthe lowest instantaneous pressures are affected first. Hence, rightatrial inversion (during ventricular systole, while the atrium is relaxed)is usually an early sign of compression, followed by diastolic compres-sion of the right ventricular outflow tract. Respiration also affectsintracardiac pressures, particularly those on the right side of the heart.During inspiration, intrathoracic and intrapericardial pressures de-crease, resulting in augmented flow into the right atrium and rightventricle, with decreased flow out of the pulmonary veins into the leftatrium and left ventricle. Reciprocal changes occur during expiration,and can be documented by Doppler echocardiographic changes inmitral and tricuspid inflow as well as pulmonary and systemic outflow
Figure 3 Large pericardial effusion, presenting as an echo-freespace anterior and posterior to the heart.
Figure 4 Large pleural effusion lies posterior to the heart andthe descending thoracic aorta (DA). The patient also has apericardial effusion (PE), which extends behind the left atrium,anterior to the descending aorta. There is also a small amountof pericardial effusion anterior to the right ventricle. AO –Ascending aorta. LA – left atrium. LV – left ventricle.
(Figure 8).18,19 In the presence of normal intrapericardial pressure,
Journal of the American Society of Echocardiography Wann and Passen 9Volume 21 Number 1
the normal respiratory variation in filling of the left and right heartcauses a small (�10 mm Hg) inspiratory decrease in systemic arterialsystolic blood pressure.
Echocardiography is a powerful tool for investigating the complexrelationships among anatomy, pressure and flow, and relative ven-tricular volume, which can be affected by interaction among thepericardium, the pleura, and the heart.20-22 When intrapericardialpressure exceeds right atrial pressure, the thin free wall of the rightatrium invaginates, collapsing toward the right atrial cavity (Figure 9).Similarly, the right ventricular free wall shows signs of collapse whenthe intrapericardial pressure exceeds right ventricular intracavitarypressure (Figure 10). Very small differences in pressure result in brieflate diastolic invagination of the right atrial free wall in the absence ofclinically significant tamponade. The longer the duration of right atrialinvagination relative to the length of the cardiac cycle, the greater thelikelihood of significant hemodynamic compromise.
Right ventricular diastolic collapse generally requires a larger pres-sure difference between the intrapericardial space and the intracar-diac chambers than does right atrial collapse. Right ventricular dia-stolic collapse is, thus, a more specific but less sensitive indicator ofhemodynamically significant pericardial compression. In experimen-tal studies, diastolic inversion of the right ventricular free wall begins
Figure 5 An echo-free clear space seen only anterior to theheart (arrow) is usually due to pericardial fat, not pericardialeffusion, as the heart “floats” in pericardial fluid.
Figure 6 An echogenic space surrounding the heart (arrow) isseen in this patient who has a bloody pericardial effusion.
abruptly. At the first appearance of right ventricular collapse, intra-
pericardial and intracardiac pressures are essentially equal, with anassociated moderate decline in stroke volume. As intrapericardialpressure increases relative to intracardiac pressure, the duration andseverity of right ventricular collapse progresses to the point of nearobliteration of the right ventricular cavity throughout diastole, andultimate circulatory collapse.
Both right atrial and right ventricular collapses are affected bychanges in the state of hydration, central blood pressure, and volume.Pulmonary hypertension and right ventricular hypertrophy can delayright ventricular collapse until very high intrapericardial pressure ispresent.21,22
Tamponade also produces reciprocal respiration-related changesin right and left ventricular volume, diastolic filling, and systolicemptying that can be documented by echocardiography. Thesefindings underlie the physiology of the exaggerated decrease insystemic aortic pressure or pulsus paradoxus that is the clinicalhallmark of tamponade. The exaggerated decrease in arterial pressureoccurs because, in the setting of a fixed intrapericardial volume, theinspiratory increase in right ventricular filling causes the interventric-ular septum to shift to the left, exaggerating the normal decrease inLV filling volume and, hence, stroke volume (ventricular interdepen-dence). With expiration, left ventricular filling and stroke volumeincrease, as right ventricular filling is relatively reduced, leading to theexaggerated variation in stroke volume and arterial pressure.
Doppler echocardiography is particularly useful in demonstratingthe exaggerated phasic variation in ventricular inflow and outflowcaused by tamponade.19 Respiratory variation in tricuspid and pul-monary flow is more dramatic than mitral and aortic flow, but thereis progressive impairment in all intracardiac flow as the degree oftamponade worsens. Plethora of the inferior vena cava is a usefulindicator of elevated right atrial pressure and is usually present in bothcardiac tamponade and constrictive pericarditis (Figure 11).
These echocardiographic findings identify changes in cardiac struc-ture and function and an associated decrease in cardiac output thatoften occur well before the onset of pulsus paradoxus and, thus, canbe an important indicator of hemodynamic compromise before itbecomes clinically apparent.
CONSTRICTIVE PERICARDITIS
Constrictive pericarditis is an uncommon, easily misdiagnosed dis-ease. Constrictive pericarditis should be in the differential diagnosisfor all patients who present with dyspnea, ascites, edema, andelevated jugular venous pressure, especially when left ventricularsystolic function is normal.
Chronic inflammation of the pericardium results in thickening,fibrosis, and fusion of both visceral and parietal layers causing im-paired diastolic cardiac filling.23 Echocardiography may be useful inrecognizing an increase in pericardial thickness (Figure 12),24 butprecise measurements are difficult because of reverberations ofreflected ultrasound or shadowing caused by calcification. The firstclue that constrictive pericarditis may be present is often the finding ofa dilated vena cava indicative of increased central venous pressure(Figure 11) in the presence of normal right and left ventricular systolicfunction. In classic constrictive pericarditis, pressures in all fourcardiac chambers equalize during diastole. At the onset of diastole,the rate of ventricular filling is often increased as a result of theelevated atrial pressures, but is rapidly arrested by the pericardialconstraint, resulting in a rapid increase in ventricular diastolic pressure
creating the characteristic dip-and-plateau pattern. Because the total
rdin
10 Wann and Passen Journal of the American Society of EchocardiographyJanuary 2008
ventricular volume is limited by the pericardium, increased filling ofone ventricle occurs at the expense of the other (ventricular interde-pendence). This ventricular interdependence underlies many of theechocardiographic signs of constriction including the respiratory shiftin the position of the interventricular septum (Figure 13), and exag-geration of the normal respiratory changes in mitral and tricuspid flow(tricuspid flow increases more than normal while mitral flow de-creases more than normal with inspiration).
Restrictive cardiomyopathy can share many of the clinical features
Figure 8 (A) Mitral valve Doppler reco
of constrictive pericarditis and a number of echocardiographic fea-
tures have been described to separate these entities. Causes ofrestrictive cardiomyopathy such as amyloid heart disease may besuggested on echocardiography when the cardiac walls are markedlythickened. Other features suggesting that a patient has restrictioninclude the presence of severe pulmonary hypertension and moresevere elevation of left ventricular filling pressures than right ventric-ular filling pressures, as these findings are not typical in constriction.
Doppler echocardiography may be especially useful in differenti-ating constrictive pericarditis from restrictive cardiomyopathy.24-32
igure 7 (A) Echocardiographically guided pericardio-entesis. The needle (arrow) is seen within the pericar-ial effusion (PE). (B) Two-dimensional echocardiogramrior to pericardiocentesis. Note echo-free spaceround the heart and invagination of the right atrial freeall. (C) Two-dimensional echocardiogram taken imme-iately after completion of pericardiocentesis, showingesolution of the pericardial effusion and no right atrialollapse.
g; (B) aortic valve Doppler recording.
Fcdpawdrc
The marked respiratory variation in left and right ventricular inflow
Journal of the American Society of Echocardiography Wann and Passen 11Volume 21 Number 1
velocities seen in constrictive pericarditis is not typically present inrestrictive cardiomyopathy. Enhanced respiratory variation in pulmo-nary vein diastolic flow may be augmented by rapid intravenousvolume loading in patients with constrictive pericarditis.
Tissue Doppler echocardiography and color Doppler M-modehave also been reported to be of value in differentiating restrictivecardiomyopathy from constrictive pericarditis.32 Em, a tissue Dopplerparameter of early relaxation, is normal in constriction, but reduced inrestriction as a result of intrinsic myocardial disease. Flow propagationvelocity into the left ventricle by color Doppler M-mode is greaterthan 45 cm/s in constriction but reduced to less than 45 cm/s in
Figure 9 A patient with a large pericardial effusion (PE) showsevidence of right atrial (RA) collapse (arrow). The right ventricle(RV), left ventricle (LV), and left atrium (LA) are normal. Rightatrial collapse by itself is not an indicator of significant hemo-dynamic embarrassment due to cardiac tamponade, but is anearly sign that intra-pericardial pressure exceeds intra-cardiacpressure.
Figure 10 Subcostal view showing pericardial effusion (PE),right atrium (RA), left ventricle (LV), and left atrium (LA).
restriction.33
EFFUSIVE CONSTRICTIVE PERICARDITIS
Effusive constrictive pericarditis combines features of cardiac tam-ponade with those of constrictive pericarditis. Figure 14 shows theechocardiogram of such a patient, who has both a large pericardial
Figure 11 (A) Subcostal two-dimensional echocardiogramshowing ascites (As) above the liver, separated from a pericar-dial effusion (PE) by the diaphragm. The inferior vena cava (IVC)is dilated as it enters the right atrium (RA), indicative of elevatedcentral venous pressure. The hepatic veins (HV) are alsodilated. (B) An M-mode echocardiogram of the inferior venacava (IVC) shows the absence of respiratory variation in thediameter of the dilated IVC.
Figure 12 Thickened pericardium (arrow) in a patient withconstrictive pericarditis.
effusion pressing on the heart and a markedly thickened pericardium
12 Wann and Passen Journal of the American Society of EchocardiographyJanuary 2008
impairing diastolic filling. Both the hemodynamic and Doppler echo-cardiographic findings may be intermediate, showing features of bothcardiac tamponade and constriction.
SUMMARY
Current widespread use of echocardiography to diagnose pericardialdisease has proven that Harvey Feigenbaum was right in his earlyenthusiasm for this technology. Ultrasound is harmless, relativelyinexpensive, and widely available. The ability of echocardiography toelucidate the functional and structural consequences of pericardialdisease is especially powerful. Although other noninvasive technolo-
Figure 13 Constrast enhanced two-dimensional echocardio-gram in a patient with constrictive pericarditis. (A) Duringinspiration the interventricular septum (IVS) curves toward theright ventricle (RV) as the left ventricle (LV) expands. (B) Duringinspiration, the interventricular septum is shifted toward the leftventricle due to fixed intrapericardial volumes, as the right heartgets larger, the left heart must get smaller.
gies including cardiac magnetic resonance and computed tomogra-
phy have been developed to provide even more detailed informationabout the heart and the pericardium, echocardiography remains thefirst and often only diagnostic method needed to make a definitivediagnosis and guide appropriate treatment in patients with pericardialeffusion, cardiac tamponade, or constrictive pericarditis. The devel-opment of echocardiography for use in pericardial disease has been alandmark development of the last half-century of cardiology.
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