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Who will benefit from this book Ideal for residents, fellows, and others who need a comprehensive, clinically focused understanding of echocardiography, The Echo Manual, 4th Edition, has been thoroughly revised with updated information, new chapters, and new video clips online. Written primarily by expert authorities from the Mayo Clinic, this best-selling reference remains a practical guide to the performance, interpretation, and clinical applications of today’s echocardiography.
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Features all-new chapters specifically devoted to 3D echo, interventional echocardiography, and hand-carried ultrasound.
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Includes new echo videos that provide a valuable learning experience of echocardiography in motion.
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Provides a concise, user-friendly summary of techniques, diagnostic criteria, and quantitative methods for echocardiography, Doppler echocardiography, and transesophageal echocardiography.
Presents complex material in an approachable, visually appealing manner that focuses on the clinical application of echocardiography as a diagnostic tool.
Covers the latest techniques, standards, and applications – all highlighted by more than 900 high-quality, annotated images that are true to gray scale and colour.
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The Echo Manual FOURTH EDITION
By Jae K.Oh, Garvan C.Kane, James B.Seward, A.Jamil Tajik
ISBN 9781496312198 Pages 528 Price £155.00
Publishing December 2018 Sample Chapter Preview
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The Echo Manual 4e By Jae K.Oh, Garvan C.Kane, James B.Seward, A.Jamil Tajik ISBN 9781496312198
Table of Contents
Chapter 1 Transthoracic M-mode and Two- dimensional Echocardiography Jae K. Oh, MD and Joseph J. Maleszewski, M.D. Chapter 2 Transthoracic Three-Dimensional Echocardiography Karima Addetia, Victor Mor-Avi, Roberto M. Lang Chapter 3 Transesophageal Echocardiography Jeremy J. Thaden, MD, Joseph F. Maalouf, MD, Jae K. Oh, MD
Chapter 9 Pulmonary Hypertension and Pulmonary Vein Stenosis Garvan Kane
Chapter 10 Cardiomyopathies
Jeffrey B. Geske, MD, Steve R. Ommen, MD and Jae K. Oh, MD
Chapter 11 Heart Failure
Garvan C. Kane MD PhD - Jae K. Oh, MD
Chapter 12 Pericardial Diseases
Ling-His Lieng, Raúl E. Espinosa, Jae K. Oh
Chapter 4 Doppler Echocardiography and
Color Flow Imaging: Comprehensive Noninvasive Hemodynamic
Chapter 13 Prosthetic Valve Evaluation
Assessment Jae K. Oh, MD
Chapter 14 Prosthetic Valve Evaluation
Lori A. Blauwet, MD, Fletcher A. Miller, MD, Jae K. Oh, MD
Chapter 5 Tissue Doppler and Strain Imaging Hector R Villarraga, MD, Garvan C. Kane, MD, Jae K. Oh, MD
Chapter 15 Infective Endocarditis
William K. Freeman, M.D., F.A.C.C., F.A.S.E.
Chapter 6 Contrast Echocardiography
Sahar S. Abdelmoneim, M.D, MSc, MS, FESE, FASE; Sharon L. Mulvagh, MD, FACC, FASE
Chapter 16 Stress Echocardiography
Robert B. McCully, MD, Patricia A. Pellikka, MD, Jae K. Oh, MD
Chapter 7 Quantification of Left-Sided Cardiac Chambers: Mass, Volumes,
Chapter 17 Coronary Artery Disease, Acute Myocardial Infarction and Tako-Tsubo Syndrome Sunil V. Mankad, MD and Jae K. Oh, MD
and Ejection Fraction Garvan C. Kane MD PhD
Chapter 8 Assessment of Diastolic Function and Diastolic Heart Failure Jae K. Oh, MD
Chapter 18 Cardiac Diseases Due to Systemic Illness, Genetics, or Medication Garvan Kane, Jae K. Oh, MD
Chapter 26 Handheld Cardiac and
Point of Care Ultrasound Michael W. Cullen, MD and Brandon M. Wiley, MD
Chapter 19 Cardiac Tumors and Masses
Chapter 27 Introduction to Echocardiography: Physics and Technique David A. Foley, MD
Kyle W. Klarich, MD, Jae K. Oh, MD, Joseph J. Maleszewski, MD
Chapter 20 Diseases of the Aorta Peter C. Spittell, MD
Chapter 28 The Future of Echocardiography
José Luis Zamorano, Ariana González, Covadonga Fernández-Golfín
Chapter 21 Congenital Heart Disease
Patrick O’Leary, Naser Ammash, and Frank Cetta
Chapter 29 Artificial Intelligence and
Echocardiography – Current Status and Future Directions David Playford MBBS FRACP PhD FCSANZ Geoff Strange BScN PhD
Chapter 22 Interventional Echocardiography Jeremy J. Thaden, MD, Brandon M. Wiley, MD Peter M. Pollak, MD, Charanjit S. Rihal, MD
Chapter 23 Adult Intra-operative Echocardiography
Hector I. Michelena, Rakesh M. Suri
Chapter 24 Intracardiac and Intravascular Ultrasound
Donald J. Hagler, Allison K. Cabalka, Guy S. Reeder
Chapter 25 Vascular Tonometry and Imaging for Cardiovascular Risk Assessment Thais Coutinho and Iftikhar J. Kullo
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The Echo Manual
CHAPTER 12
Pericardial Diseases Ling-His Lieng, Raúl E. Espinosa and Jae K. Oh
Acquired abnormalities of the pericardium include inflammation, effusion, neoplasia, fibrosis, and calci- fication, which can manifest clinically as chest pain, dyspnea, heart failure, hypotension, and even cardio- genic shock. Other structural abnormalities include con- genital absence of the pericardium and pericardial cyst. Echocardiography is the most important clinical tool in the recognition and management of these pericardial diseases. Detection of pericardial effusion was the first clinical application of echocardiography, using an “A” (amplitude) mode in 1963 (4) (see Fig. XX). This tech- nique subsequently revolutionized the diagnosis of peri- cardial effusion and tamponade and is now routinely used to safely guide pericardiocentesis (5). Comprehensive 2D and Doppler echocardiography is also fundamental in the diagnosis of constrictive pericarditis (6,7). When trans- thoracic imaging windows are unfavorable, transesoph- ageal echocardiography (TEE) can help in measuring pericardial thickness (8), detecting loculated pericardial effusion or other structural abnormalities of the peri- cardium, and evaluating diastolic function for tampon- ade or constrictive physiology. Three-dimensional (3D) echocardiography may in some cases yield incremental information to 2D imaging. The various applications of echocardiography in the evaluation of pericardial dis- eases are illustrated in this chapter. CONGENITALLY ABSENT PERICARDIUM Congenital absence of the pericardium is a rare disorder, which usually involves complete absence of the left side of the pericardium. Absence of the right hemopericardium :ROWHUV .OXZHU ,QF 8QDXWKRUL]HG UHSURGXFWLRQ R I WKH FRQWHQW LV SURKLELWHG Q1 Q2
The normal pericardium, which has an anatomic thick- ness of ≤ 1 to 2 mm (1), consists of an outer layer called the fibrous pericardium and an inner layer called the serous pericardium. The visceral layer of the serous peri- cardium, or epicardium, covers the heart and proximal great vessels. There is varying amount of fat between the myocardium and the epicardium. It is reflected to form the parietal pericardium, which lines the fibrous peri- cardium (Fig. 12-1). The reflections of the serous pericar- dium between the arteries and the veins form sinuses and recesses (Fig. 12-2). The pericardium provides mechanical protection for the heart and exerts notable hemodynamic effects on the atria and ventricles. The finite compliance of the normal pericardium limits cardiac chamber disten- tion. Ventricular volume is greater at any given ventricular filling pressure with the pericardium removed than with the pericardium intact. Through the same mechanism, the pericardium also promotes diastolic coupling, or inter- dependence, between the two ventricles. The increased filling of one ventricle reduces the filling of the other. This phenomenon underlies the pathophysiology of car- diac tamponade and constrictive pericarditis. Apart from these mechanical functions, the pericardial mesothe- lium produces 25 to 50 mL of fluid, which has lubricant, anti-infective, fibrinolytic, and paracrine properties. Fat deposited around the pericardium, specifically epicardial fat, reflects visceral adiposity and may be a marker of car- diometabolic risk factors (2). Pericardial fluid is drained by the lymphatic system, and venous drainage is provided by pericardiophrenic veins that drain into the innomi- nate veins (3). The pericardium has extensive autonomic innervation.
Fig. 12-1
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FIGURE 12-1 Pathology specimens showing the double-layered pericardium with (left) and without (right) the heart in the fibrous pericardial cavity. (Courtesy W. D. Edwards, MD.)
the pericardium, the angle between the ultrasound beam and the left ventricular posterior wall (Angle − PW) at end-diastole from the parasternal long axis view and the distance between the chest wall and the most distal part of the left ventricular posterior wall (Distance − PW) from the parasternal mid-ventricular short axis view in the left and right decubitus positions can help confirm this anatomical defect (10) (Fig. 12-4). Thus, absence of the pericardium is readily recognized by these typi- cal 2D echocardiographic features and can be confirmed with computed tomography (CT) or magnetic resonance imaging (MRI) (Fig. 12-3C). PERICARDIAL CYST A pericardial cyst is a thin-walled, loculated structure filled with clear fluid (hence “spring water cyst”), usually detected as an incidental mass lesion on chest radiogra- phy or as a cystic mass on echocardiography (Fig. 12-5A). Pericardial cysts must be differentiated from loculated pericardial effusion, cardiac chamber enlargement, diaphragmatic hernia, and malignant tumors. Two- dimensional echocardiography can readily differenti- ate the echo-free content of a pericardial cyst from solid structures. The typical location of pericardial cysts in the right cardiophrenic angle is another clue, although
and complete absence of the pericardium are uncommon. It often occurs in isolation but can be associated with atrial septal defect, bicuspid aortic valve, and broncho- genic cysts. Although generally asymptomatic, partial defects in particular may cause dyspnea, chest pain (sometimes positional), syncope, or even sudden cardiac death as a result of herniation and torsion or strangulation of the heart and great vessels. Cardiac motion is exaggerated, especially the posterior wall of the left ventricle (LV). With complete absence of left pericardium, the most common situation, the heart is shifted to the left, with the apex displaced toward the axilla. Consequently, lung tissue is trapped between the descending thoracic aorta and the pulmonary artery, which along with the straight- ened left heart border creates a “Snoopy Dog” appear- ance on chest X-ray (Fig. 12-3A). The right ventricular (RV) cavity appears enlarged from the standard paraster- nal window, mimicking RV volume overload, and is situ- ated in the center of the standard apical window, with the interventricular septum deviated leftward (Fig. 12-3B and C). The combination of bulbous ventricles and elon- gated atria, as the heart is suspended from its vascular pedicle, gives rise to a “tear-drop heart” appearance in the apex down apical format (9). Since the heart moves more readily (”pendulum heart”) (9) without a portion of &RS\ULJKW
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FIGURE 12-2 A: The anterior portion of the pericardial sac and the heart have been removed. This view exposes the lateral, dorsal, and diaphragmatic aspects of the pericardial sac. The visceral and parietal pericardium are con- tinuous at the basal region of the heart, where the great arteries and veins are located. The aorta and pulmonary trunks are enclosed in one sheath, while the pulmonary veins and venae cavae are covered separately. B: The trans- verse sinus ( black arrow path ) is the space between the arterial and venous pericardial reflections that form an access path between the right and left sides of the pericardial cavity. The cul-de-sac behind the left atrium bounded by the pulmonary veins is called the oblique sinus ( white interrupted line area ). Ao , aorta; LPA , left pulmonary artery; LPV , left pulmonary veins; RPA , right pulmonary artery; RPV , right pulmonary veins; SVC , superior vena cava. (B) The heart is shown with only a rim of the pericardium left and marked by the arrows. The transverse sinus is indicated by the asterisks as shown from the right and left sides of the heart. (From Klein AL, Abbara S, Agler DA, et al. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of patients with pericardial disease: Endorsed by the Society for Cardiovascular Magnetic Resonance and Society of Cardiovascular Computed Tomography. Journal of the American Society of Echocardiography, 2013;26:965–1012 e15, with permission.)
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FIGURE 12-3 A: Chest X-ray of congenital absence of the left pericardium, with an “Snoopy Dog” appearance. Because of the absent pericardium, lung tis- sues ( arrow ) are trapped between the descending aorta and pulmonary artery, mimicking the ear of a snoopy dog. B: Parasternal long ( left ) and apical ( right ) views of the heart with congenital absence of the perica- dium. Because of the leftward shift of the heart, the right ventricle ( RV ) is at the center of the apical image rather than the left ventricular ( LV ) apex; this is often confused with RV volume overload. Cardiac catheterization was performed elsewhere to evaluate an atrial septal defect and showed no shunt before this evaluation. LA , left atrium; RA , right atrium (Video 12-1). C: MRI appearance of congenital absence of the pericardium. Most of the left side pericardium is missing (between two arrows ), and the heart is rotated leftward through the pericardial defect.
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PERICARDIAL EFFUSION AND TAMPONADE Accumulation of fluid or blood in the potential pericar- dial space results in a pericardial effusion, detected as an echo-free space. When the effusion exceeds 25 mL, this echo-free space persists throughout the cardiac cycle. A trivial, potentially physiologic pericardial effusion is a posterior echo-free space that is present only during sys- tole. An effusion is deemed small if the pericardial space is less than 1 cm wide in diastole, moderate if 1 to 2 cm,
they can also be found in the left cardiophrenic angle (Fig. 12-5B), hilum, and superior mediastinum. While usually benign and asymptomatic, pericardial cysts may enlarge and cause compression of the heart and adja- cent structures (11). Drainage of cystic fluid is usually not curative since it reaccumulates, and thoracoscopic or surgical removal is necessary when the cyst becomes symptomatic. CT and MRI can verify the diagnosis and help guide intervention if indicated (Fig. 12-5A and B). &RS\ULJKW 1
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FIGURE 12-4 Angle-PW in patients with CAP was significantly greater than in those with ASD (100.1 ± 12.5 degrees vs. 74.5 ± 8.6 degrees, p < 0.017) or in normal subjects (100.1 ± 12.5 degrees vs. 69.9 ± 7.6 degrees, p < 0.017) at the left decubitus, and the difference in Angle-PW according to posture (left vs. right) was significantly greater in CAP compared with the other groups (CAP 20.7 ± 12.7 degrees, ASD 0.31 ± 1.80 degrees, normal 0.31 ± 1.40 degrees, all p < 0.017). The differences in Distance-PW according to patient position (CAP 2.43 ± 0.77 degrees, ASD 0.42 ± 0.45 degrees, normal 0.26 ± 0.55 degrees) or cardiac cycle in each position (left: CAP 1.60 ± 0.76 degrees, ASD 0.41 ± 0.27 degrees, normal 0.17 ± 0.12 degrees; right: CAP 0.70 ± 0.32 degrees, ASD 0.22 ± 0.19 degrees, normal 0.22 ± 0.13 degrees) were significantly higher in the CAP group than in the other groups (all p < 0.017).
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FIGURE 12-5 A: Chest X-ray (with arrows in left ), MRI ( upper right ), and subcostal echo- cardiographic view showing a large pericardial cyst (*) adjacent to the right atrium ( RA ). It has a typical echo-free appearance, with a smooth border. LV , left ventricle; RV , right ventricle. B: Chest X-ray (with arrows in upper left ), MRI (* in upper right ), 2-dimensional and 3-dimensional ( lower right ) imaging of a large pericardial cyst. * indicates the pericardial cyst (Video 12-2).
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FIGURE 12-6 Parasternal long-axis views showing a large pericardial effusion with swing- ing motion of the heart due to a large amount of pericardial effusion. When the LV cavity is close to the surface ( left ), the QRS voltage increases on the electrocardiogram ( bottom ), but it decreases when the LV swings away from the surface ( right ), producing electrical alternans. LV , left ventricle; RV , right ventricle (Video 12-3).
in ventricular chamber size, and plethora of the inferior vena cava with blunted inspiratory collapse (Fig. 12-8). Cardiac chamber collapse occurs when intrapericardial pressure exceeds intracardiac pressure and therefore is most evident in diastole when cardiac pressure is reduced, in the more compliant right heart chambers. Right atrial (RA) inversion during the late diastole is an early but non- specific sign of cardiac tamponade. It is sometimes seen in hypovolemia and must be distinguished from nor- mal atrial systole. Corroborative evidence of tamponade should be sought if RA buckling is transient (14). The spec- ificity of RA collapse for tamponade is high if it persists for ≥ 1/3 of the cardiac cycle and extends into ventricular
large if greater than 2 cm, and very large if greater than 2.5 cm (1). Small pericardial effusions are often localized posteriorly; moderate or larger effusions are frequently circumferential. The specific etiology of pericardial effu- sion is not usually evident on echocardiography except for coagulum or air in the pericardial sac. However, large effusions are often seen with malignancy, tuberculosis, hypothyroidism, and uremia, while effusions associ- ated with heart failure are usually small. It is important to investigate the etiology of a pericardial effusion, but many effusions remain idiopathic. As a pericardial effusion enlarges, increasing intraperi- cardial pressure reduces the myocardial transmural pres- sure (i.e., intracardiac pressure−intrapericardial pressure). This same effect can occur with extrinsic compression, for instance, from a large pleural effusion (12,13). Tamponade occurs when the intrapericardial pressure increases to the point of compromising systemic venous return to the right heart, reducing cardiac output. When an effusion is very large, the heart may have a “swinging” motion within the pericardial cavity (Fig. 12-6), which accounts for the elec- trocardiographic (ECG) manifestation of cardiac tampon- ade called electrical alternans (Fig. 12-6, bottom panel). However, a swinging heart is not always present in cardiac tamponade, which can occur when a smaller pericardial effusion accumulates quickly, such that the pericardium has no time to stretch and accommodate the effusion (12). The intrapericardial pressure and volume relationship is much steeper under these circumstances (Fig. 12-7), for exam- ple, following myocardial perforation in acute myocardial infarction or in aortic dissection. With increasing interven- tional and electrophysiology procedures for structural heart disease and complex arrhythmias, respectively, cardiac perforation with hemopericardium and acute tamponade occurs more frequently, resulting in hypotension and the need for prompt pericardiocentesis. M-mode and 2D echocardiographic signs of tampon- ade include cardiac chamber compression, respirophasic abnormal ventricular septal motion, respiratory variation
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FIGURE 12-7 Pericardial pressure-volume (or strain- stress) curves of cardiac tamponade showing volume increases slowly or rapidly over time. Left , Rapidly increas- ing pericardial fluid first reaches the limit of the pericar- dial reserve volume (the initial flat segment) and then quickly exceeds the limit of parietal pericardial stretch, causing a steep rise in pressure, which becomes even steeper as smaller increments in fluid cause a dispro- portionate increase in the pericardial pressure. Right , A slower rate of pericardial filling takes longer to exceed the limit of pericardial stretch because there is more time for the pericardium to stretch and for compensatory mechanisms to be activated. (From Spodick [9], used with permission.) Q4
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FIGURE 12-8 A: Left , 2-D and M-mode echocardiogram of plethoric inferior vena cava ( IVC ), which is present in most of patients with cardiac tampon- ade. Right , M-mode echocardiogram from the parasternal window in a patient with cardiac tamponade and a large circumferential pericardial effusion ( PE ). The M-mode was recorded simultaneously with the respirometer tracing at the bottom ( upward arrow , onset of inspiration; downward arrow , onset of expiration). The left ventricular dimension during inspiration becomes smaller than with expiration. The opposite changes occur in the right ventricle. The ventricular septum moves toward the LV with inspiration and toward the RV with expiration, accounting for the abnormal ventricular septum in patients with cardiac tamponade. B: A subcostal view of a plethoric IVC ( upper left ), M-mode of RV-free wall with early diastolic collapse ( arrow in lower left ), hepatic vein Doppler showing diastolic flow reversals with expiration ( arrow in upper right ), and mitral inflow velocity with respiratory variation ( lower right ). Note that mitral E velocity is lower than A velocity in most of patients with pure tamponade. :R O W H U V . O X Z H U , Q F 8 Q D X W K RU L ] H G U H S U R G X F W L R Q R I W K H FRQW
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systole. Compared to RA diastolic collapse, RV collapse in early diastole is very specific for tamponade. Diastolic compression of the right heart may be absent if right- heart pressure is elevated. Left atrial (LA) chamber col- lapse is uncommon but very specific for tamponade, and LV collapse is rare. Abnormal ventricular septal motion results from respiratory variation in ventricular filling (see discussion below). Plethora of the inferior vena cava with impaired inspiratory compression indicates elevated RA pressure from high intrapericardial pressure, but a subset of the patients with clinical tamponade may lack IVC plethora and inspiratory compression. (Miranda et al. Unpublished observation). With acute myocardial rupture or proximal aortic dis- section, echodense clotted blood (hemopericardium) may accumulate in the pericardial sac; this finding is called coagulum tamponade (Fig. 12-9). When air devel- ops in the pericardial sac (pneumopericardium) as a result of esophageal perforation, transthoracic and TEE are difficult because ultrasound does not penetrate air well, but localized pneumopericardium has a characteris- tic appearance (Fig. 12-9). The Doppler echocardiographic findings of pericardial effusion with hemodynamic compromise are more sensi- tive than the 2D echocardiographic features mentioned above (15,16). They result from changes in the left ventricu- lar filling gradient mediated by respirophasic intrathoracic pressure changes and amplified by increased ventricular interdependence, or increased dependence of LV filling on RV filling (and vice versa) within the relatively fixed total cardiac volume (17). Similar to constrictive pericarditis Q7
FIGURE 12-8 ( Continued ) C: Top , Parasternal long-axis views during systole and diastole of a patient with tamponade. During early diastole, the RV-free wall col- lapses ( arrows at top ). LA , left atrium; VS , ventricular septum; LV , left ventricle; RV , right ventricle. Bottom , Apical four-chamber view demonstrating late diastolic collapse of right atrial ( RA ) wall ( arrow ). This sign is sensitive but not specific for tamponade. When RA inversion lasts longer than a third of the RR interval, it is specific for tamponade.
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FIGURE 12-9 Left: A subcostal view showing echodense gelatinous mass ( arrows ) in the pericardial sac characteristic for hemopericardium (Video 12-4). Right: Bright echoreflection ( arrows ) in the pericardium characteristic for pneumoperi- cardium in a patient with gastropericardial fistula. LA , left atrium; RA , right atrium; RV , right ventricle.
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FIGURE 12-10 Pulmonary vein and hepatic vein Doppler patterns of tampon- ade. A: Diastolic forward pulmonary venous flow decreases ( single arrowhead ) after inspiration ( Insp ) and increases ( double arrowheads ) after expiration ( Exp ). B: The hepatic vein has a marked decrease in diastolic forward flow and an increase in diastolic reversals ( DR ) after expiration. D , diastolic flow; S , systolic flow. (From Oh JK, Hatle LK, Mulvagh SL, et al. Transient constric- tive pericarditis: Diagnosis by two-dimensional Doppler echocardiography. Mayo Clinic Proceedings, 1993;68:1158–1164. Used with permission of Mayo Foundation for Medical Education and Research.)
valves are also reflected in the pulmonary and hepatic venous flow velocities as follows: an inspiratory decrease and an expiratory increase in pulmonary vein diastolic forward flow and an expiratory decrease in hepatic vein forward flow and an expiratory increase in expiratory reversal flow (Fig. 12-10). The presence of these typical Doppler velocity changes indicates hemodynamic com- promise due to pericardial effusion. Although there is a similarity between constriction and tamponade in terms of respiratory variation in ventricular filling, these filling patterns are different. In tamponade, due to increased intrapericardial pressure with decreased transmural pres- sure gradient, LV and RV filling are impeded throughout diastole, more so during early diastole, manifesting as a low mitral E velocity and E/A reversal (<0.8). In constric- tion, ventricular filling is generally restrictive (see below). Cardiac tamponade is relieved by removal of the peri- cardial fluid. Although pericardiocentesis is lifesaving, a blind percutaneous approach has a relatively high rate of complications, including pneumothorax, puncture of the cardiac wall, and death. Two-dimensional echocardiogra- phy can identify the optimal site of puncture (Fig. 12-11) by determining the thickness of the pericardial effusion envelope and its distance from the puncture site as well as monitor the results of the pericardiocentesis, usually from the subcostal window. The appropriate position of the peri- cardiocentesis needle within the pericardial space can be confirmed by imaging during injection of agitated saline. Figure 12-12 shows contrast in the pericardial space, not in the RV. At Mayo Clinic, most pericardiocentesis proce- dures are performed with 2D echocardiographic guidance. The most common locations for needle entry are the para- ECHOCARDIOGRAPHICALLY GUIDED PERICARDIOCENTESIS
(see below), the inspiratory fall of intrathoracic pressure is not fully transmissible to the LV in the presence of peri- cardial fluid (18). Thus, the pressure gradient for LV fill- ing is reduced. In contrast to constriction, where LV filling occurs primarily during early diastole (with the greatest limitation to filling occurring from mid to late diastole), LV filling in pure tamponade (without effusive-constrictive pericarditis) is impaired or reduced during early diastole due to increased intrapericardial pressure, and late filling with atrial contraction is increased (Fig. 12-8B). Moreover, during inspiration, the fall of intrapleural pressure aug- ments systemic venous return. Due to impairment in the right heart’s capacity to dilate from the effusion and the concurrent reduction in LV filling gradient during inspira- tion, the interventricular septum shifts from right to left to accommodate the increase in systemic venous return. During expiration, less venous return to the right heart and recovery of the LV pressure gradient for filling shift the septum rightward, increasing LV filling. Consequently, LV stroke volume and systolic BP are reduced during inspira- tion, and vice versa during expiration. Competitive filling of the RV and LV during respiration forms the basis for pulsus paradoxus in cardiac tamponade. In constriction, increased ventricular interdependence is initiated by the respiratory variation in left ventricular filling, as opposed to RV filling in tamponade (19). The reciprocal changes in mitral and tricuspid flow velocities in tamponade are closely coupled to respira- tory phase and therefore greatest on the first beats of inspiration and expiration. Defining percentage velocity change as [(velocity in expiration − velocity in inspira- tion)/velocity in expiration], the American Society of Echocardiography has recommended these thresholds as diagnostic of tamponade: a 30% change in mitral E veloc- ity and 60% change in tricuspid E velocity (1). Respiratory changes in flow velocity across the mitral and tricuspid &RS\ULJKW
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FIGURE 12-11 (See Video A and B) Echocardiographically guided pericardiocentesis (Video 12-5). Step 1. Locate an area on the chest or subcostal region from which the largest amount of pericardial effusion can be visualized and mark it ( A – C ). Step 2. Determine the depth of effusion from the marked position and the optimal angulation. Step 3. After sterile preparation and local anesthesia, perform pericardiocen- tesis ( D ). Step 4. When in doubt about the location of the needle, inject saline solution through the needle and image it from a remote site to locate the bubbles. Step 5. Monitor the completeness of the pericardiocentesis with repeat echocardiography. Step 6. Place a 6F or 7F pigtail catheter in the pericardial space to minimize reac- cumulation of fluid ( E ). Step 7. Drain any residual fluid or fluid that has reaccumulated via the pigtail catheter every 4–6 hours. If after 2–3 days pericardial fluid has not reac- cumulated, as seen in echocardiographically, the pigtail catheter may be removed. Always have the pericardial fluid analyzed: cell counts, glucose and protein measurements, culture, and cytology. (Modified from Callahan JA, Seward JB, Tajik AJ, et al. Pericardiocentesis assisted by two-dimensional echocardiography. Journal of Thoracic and Cardiovascular Surgery, 1983:85:877–879, used with permission.)
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This approach has markedly curtailed the rate of recurrent effusion and need for a sclerosing agent. Rapid drainage of large volumes of pericardial fluid should be avoided as a “pericardial decompression syndrome,” character- ized by hemodynamic deterioration, pulmonary edema, or ventricular dysfunction, can ensue (21). For recurrent malignant pericardial effusion, there are no uniform approaches, and options may include repeat pericardio- centesis and drainage, surgical creation of a pericardial window, percutaneous balloon pericardiotomy, intraperi- cardial sclerosis or steroid instillation, and local or sys- temic chemotherapy. Pericardial effusions are usually circumferential. If the echo-free space is found only anteriorly, it may represent epicardial fat rather than a pericardial effusion. Posteriorly, a pericardial effusion is anterior to the descending tho- racic aorta, whereas a left pleural effusion is posterior to the aorta (Fig. 12-13). Two-dimensional ultrasonographic imaging of a pleural effusion prior to thoracentesis is helpful in locating the optimal puncture site. A left pleu- ral effusion allows cardiac imaging from the back. PERICARDIAL FAT Pericardial fat is common and often mistaken for peri- cardial effusion. Fat is usually present anteriorly over the right ventricle, with no posterior echolucent space, unlike the typical posteriorly located small pericardial effusion. Less commonly, pericardial fat deposition may be more extensive. Other distinguishing features of pericardial fat include a stippled appearance (Fig. 12-14) and some y PERICARDIAL EFFUSION VERSUS PLEURAL EFFUSION
sternal or apical areas; the subxiphoid location is used less frequently. In 1,127 consecutive echocardiographically guided pericardiocentesis procedures in our laboratory (20), malignant effusion was the most common reason for the procedure (34% of cases), followed by a postoperative complication (25%), complication of a catheter-based pro- cedure (10%), and miscellaneous causes. The procedure was successful in 97% of patients. Major complications were rare (1.2%) and included death (1 patient), cardiac laceration (5), vessel laceration (1), pneumothorax (5), infection (1), and sustained ventricular tachycardia (1). Typically, a pigtail catheter (6F or 7F) is introduced and left in the pericardial sac for about 3 days, with intermit- tent drainage every 4 to 6 hours. Once daily fluid drainage is less than 50 mL and a repeat echocardiogram con- firms absence of reaccumulation, the catheter is removed. FIGURE 12-12 The appearance of agitated saline ( arrows ) in the pericardial sac. If agitated saline is seen in any car- diac chamber, surgical consultation should be obtained immediately before any attempt is made to remove the pericardiocentesis needle or catheter.
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FIGURE 12-13 Two-dimensional imaging of pleural effusion ( PL ) from the parasternal (A) and apical (B) long-axis views. A pericardial effusion is present between the descending thoracic aorta ( Ao ) and the posterior cardiac walls, whereas a pleural effusion is present behind the descending thoracic aorta. LA , left atrium; LV , left ventricle; RV , right ventricle.
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more common diseases. Because constrictive pericardi- tis is potentially curable, it should be considered in all patients with heart failure, especially those with normal or relatively preserved ejection fraction and predispos- ing factors for the disease. In the United States, the most common identifiable causes of constriction are previous cardiac surgery, an antecedent episode of acute pericardi- tis, and radiotherapy (23,24). These causes highlight the importance of iatrogenic constrictive pericarditis, which may become more prevalent as a greater number of com- plex, catheter-based (including epicardial), electrophysi- ological, and structural cardiac procedures are attempted (25). Patients with constrictive pericarditis present with dyspnea, peripheral edema, ascites, pleural effusion, fatigue, or anasarca. The jugular venous pressure is almost always elevated, with a characteristic rapid “y” descent (Fig. 12-16). Other notable physical findings include Kussmaul sign and pericardial knock. The nadir of the “y” descent corresponds to the timing of a pericardial knock. Because ascites and elevated liver enzymes from hepatic venous congestion occur frequently with constriction, FIGURE 12-16 Simultaneous jugular venous pressure ( JVP ) tracing and pulsed wave Doppler recording of hepatic vein ( HV ) velocities. There is the characteristic y descent. D , diastolic flow; S , systolic flow; x and y , jugular venous pressure wave forms.
FIGURE 12-14 Parasternal long-axis view of a thick layer of epicardial fat ( arrows ). Ao , aorta; LA , left atrium; LV , left ventricle; RV , right ventricle.
mobility in tandem with the underlying myocardium. Two layers of fat may be identifiable—epicardial fat, which is beneath the epicardium and surrounds the epicardial coronary arteries, and paracardial fat, which is external to the parietal pericardium (22). Epicardial (rather than paracardial) fat correlates with visceral adiposity, meta- bolic syndrome, cardiovascular risk factors, and prevalent coronary artery disease (2). CONSTRICTIVE PERICARDITIS Constrictive pericarditis results from an adherent, inflamed, fibrotic, or calcified pericardium that limits dia- stolic filling of the heart (Fig. 12-15). Though not uncom- mon, constrictive pericarditis is frequently overlooked because the clinical presentation mimics that of other ar
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FIGURE 12-15 Heart specimens from two patients who died with constrictive pericarditis. A: The peri- cardium is thickened and calcified. B: The pericardial thickness is relatively normal but adherent to the epicardium. In both cases, diastolic filling of the right- and left-heart chambers was markedly reduced.
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namic abnormalities specific to constriction and include comprehensive echocardiography (6,7,26,31,32) and inva- sive hemodynamic cardiac catheterization, with simultane- ous recording of the respiratory cycle (33,34). The M-mode and 2D echocardiographic features of constrictive pericarditis include a thickened pericardium, respirophasic abnormal ventricular septal motion, flat- tening of the LV posterior wall during diastole, respiratory variation in ventricular size, and a dilated inferior vena cava (Fig. 12-18). However, these findings are not decisive for the diagnosis. Hatle and colleagues (31) described the seminal Doppler features of constriction that are distinct from those of restrictive myocardial disease. They reflect the following pathophysiologies: 1) dissociation between intrathoracic and intracardiac pressures and 2) exagger- ated ventricular interdependence. To establish the diag- nosis of constrictive pericarditis, these two hemodynamic disorders must be demonstrated. A noncompliant, adherent pericardium prevents full transmission of the intrathoracic pressure changes that occur with respiration to the intracardiac cavities. With inspiration, intrathoracic pressure falls (normally 3–5 mm Hg) and the pressure in other intrathoracic struc- tures (pulmonary veins, pulmonary capillaries) decreases to a similar degree. Since the noncompliant pericardium shields the cardiac chambers from this inspiratory pressure decline, the pressure difference between the pulmonary n
many patients undergo noncardiac procedures such as liver biopsy, endoscopy, and even abdominal exploration for suspected liver or other gastrointestinal disease before constrictive pericarditis is diagnosed. Confirmation of constrictive pericarditis had been chal- lenging, but with the application of blood flow and tissue velocity Doppler imaging as well as M-mode and 2-D echo- cardiography, constrictive pericarditis can be diagnosed and distinguished from myocardial disease with high sensitiv- ity and specificity (26). In contrast, pericardial calcification on chest radiography occurs in only 23% of patients (27) (Fig. 12-17). The identification of a thick pericardium by tomographic imaging is typical with constriction, but peri- cardial thickness may be normal in nearly 20% of patients (28). Furthermore, a thickened or calcified pericardium does not by itself indicate hemodynamically significant constriction. Traditional invasive hemodynamic abnor- malities of constriction may overlap with those of restric- tive cardiomyopathy or other intrinsic myocardial diseases (29). B-type natriuretic peptide levels tend to be lower (or even normal) in constrictive pericarditis than in restrictive myocardial disease but cannot reliably distinguish the two disorders, particularly in patients with mixed myocardial and pericardial diseases (30). Thus, the diagnosis of con- striction should be based on its characteristic hemodynam- ics. The diagnostic studies, which most reliably identify constrictive pericarditis, detect the respirophasic hemody-
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FIGURE 12-17 Lateral ( left ) and posteroanterior ( right ) chest radiographs showing pericardial calcification ( arrows ). Calcification is most common in the diaphragmatic portion of the pericardium.
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FIGURE 12-18 A: Typical M-mode echocardiograms of constrictive pericarditis ( top ) and tamponade ( bottom ). Note the typical respiratory shift of the ventricular septal motion toward the left ventricle ( LV ) with inspiration ( upward arrow ) and toward the right ventricle ( RV ) with expiration ( downward arrow ) in both conditions (Video 12-6). This is a result of increased interventricular depen- dence. B: In constriction, the posterior wall is flattened soon after early dias- tole ( arrow at top ). In tamponade, the posterior wall does not have the early diastolic flattening ( arrow at bottom ).
and LV filling recovers with expiration. This characteristic hemodynamic pattern is best illustrated by simultaneous pressure recordings from the LV and pulmonary capil- lary wedge in combination with mitral inflow velocities (Fig. 12-19).
veins and LA decreases immediately after inspiration, reducing left heart filling. Consequently, mitral valve opening is delayed, which lengthens the isovolumic relaxation time (IVRT) and decreases the mitral inflow E velocity. Conversely, the pressure gradient driving LA
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FIGURE 12-19 A: Simultaneous pressure recordings from the left ventricle ( LV ) and pulmo- nary capillary wedge together with mitral inflow velocity on a Doppler echo- cardiogram. The onset of the respiratory phase is indicated at the bottom. EXP , expiration; INSP , inspiration. With the onset of expiration, pulmonary capillary wedge pressure ( PCW ) increases much more than LV diastolic pres- sure, creating a large driving pressure gradient ( large arrowhead ). With inspira- tion, however, PCW decreases much more than LV diastolic pressure, with a very small driving pressure gradient ( three small arrowheads ). These respira- tory changes in the LV filling gradient are well reflected by the changes in the mitral inflow velocities recorded on Doppler echocardiography. B: Diagram of a heart with a thickened pericardium to illustrate the respiratory variation in ventricular filling and the corresponding Doppler features of the mitral valve, tricuspid valve, pulmonary vein ( PV ), and hepatic vein ( HV ). These changes are related to discordant pressure changes in the vessels in the thorax, such as pulmonary capillary wedge pressure ( PCW ) and intrapericardial ( IP ) and intracardiac pressures. Hatched area under curve , reversal of flow; thicker arrows , greater filling; D , diastolic flow; LA , left atrium; LV , left ventricle; RA , right atrium; RV , right ventricle; S , systolic flow (Video 12-7).
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than 40% in tricuspid E velocity, and increased diastolic flow reversal with expiration in the hepatic vein should be demonstrated to establish the diagnosis of constrictive pericarditis (1) (Fig. 12-20). Thus, the patterns of respira- tory variation in LV and RV filling are similar to those in cardiac tamponade, though the initiating event in the ventricular interdependence is different between two conditions (19). In up to 50% of patients with constrictive pericarditis, the respiratory variation in mitral E velocity may be less than 25% (36). This observation could reflect: 1) lower sensitivity of mitral E velocity variation in detecting more severe constriction when LA pressure is markedly increased and 2) mixed constriction and restriction physiology. When LA pressure is markedly increased from severe constriction, mitral valve opening occurs on the steep portion of the LV pressure curve, where respiration has little effect on the transmitral pressure gradient (37). Historically, Doppler echocardiography was repeated after preload reduction maneuvers, such as head-up tilt or assumption of the sit- ting position (37). However, this maneuver is rarely neces- sary now since the application of tissue Doppler imaging of mitral annulus longitudinal motion can identify con- striction in the absence of respiratory variation in mitral inflow velocities. As emphasized below, constrictive peri- carditis should be suspected when the mitral annulus early diastolic medial (e ′ ) velocity is preserved ( ≥ 8 cm/s) in patients with clinical evidence of heart failure, especially in the setting of a restrictive LV filling pattern (i.e., mitral E/A ≥ 1.5, deceleration time <160 milliseconds). Tissue Doppler imaging of mitral annular diastolic longitudinal velocity reveals contrasting findings in
Diastolic filling (or distensibility) of the LV and RV is mutually dependent because the overall cardiac volume is relatively fixed within the noncompliant and adher- ent pericardium. Hence, reciprocal respiratory changes occur in the filling of the LV and RV. With inspiration, the decreased filling in the LV described above allows for increased filling in the RV to accommodate augmented venous return. This increased ventricular interaction manifests itself by a leftward shift of the ventricular sep- tum and an exaggerated increase in the tricuspid inflow E velocity and hepatic vein diastolic forward flow veloc- ity (Fig. 12-20). With expiration, LV filling recovers and systemic venous return decreases, causing the ventricular septum to shift to the right, limiting RV filling. Tricuspid inflow E velocity decreases and hepatic vein diastolic forward flow decreases, with pronounced flow reversal during diastole. Typically, hepatic vein diastolic forward flow velocity is higher than systolic forward flow velocity, corresponding to the systemic y and x venous waveforms, respectively. Respiratory variation in the pulmonary valve regurgitation Doppler profile, arising from dissociation of pressures within the intrathoracic pulmonary artery and the encased RV, also occurs (35). An inspiratory decrease in pressure within pulmonary artery reduces the pulmo- nary artery − RV pressure gradient, resulting in early dia- stolic cessation of regurgitation during inspiration. This Doppler echocardiographic sign has relatively low sensi- tivity and specificity for the diagnosis of constrictive peri- carditis (35). Using the same formula for calculating percent veloc- ity change as in tamponade, a respiratory variation of greater than 25% in the mitral inflow E velocity, greater
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FIGURE 12-20 Typical mitral inflow and hepatic vein pulsed wave Doppler recordings in constrictive pericarditis along with simultaneous recording of respiration ( bottom ) (onset of inspiration at upward deflection and onset of expiration at downward deflection). Left: The first mitral inflow is at the onset of inspiration, and the fourth mitral inflow is soon after the onset of expiration. Mitral inflow E velocity is decreased with inspiration (1st and 6th beats). Right: With expiration, there is a marked diastolic flow reversal ( arrow ) in the hepatic vein (6th beat soon after the downward deflection of respirometer recording). Insp , inspiration; Exp , expiration.
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FIGURE 12-21 A figure of apical long axis view showing early diastolic motion of the medial mitral annulus ( downward arrows with dotted box ) in normal individual, patient with impaired relaxation in myocardial disease, and constrictive peri- carditis. Early diastolic mitral annulus velocity ( downward arrow ) is decreased in myocardial diseases and preserved or increased in contrictive pericarditis (Video 12-8). LV , left ventricle; RV , right ventricle. XWKRUL]HG UHSURGXFWLRQ RI WKH FRQWHQW LV SURKLELWHG GXFW
also been shown that the thickness of the pericardium at the atrioventricular groove is inversely proportional to the respective lateral e ′ velocity (42). Both septal and lateral LV e ′ velocity decrease after pericardiectomy (41). The reduc- tion in septal e ′ is proportionately greater, thus normaliz- ing the ratio between septal and lateral e ′ and abolishing annulus reversus. Myocardial tethering to the pericardium is also appar- ent with strain imaging of regional LV systolic function in patients with constrictive pericarditis. The inferior and lateral walls, which are tethered to the pericardium, show reduced longitudinal strain, while the ventricular septum maintains normal strain values (Fig. 12-23).
constriction versus restrictive myocardial disease (7,26,32) (Fig. 12-21). In almost all, if not all, myocardial disease, LV relaxation is impaired, so mitral annulus e ′ velocity, which reflects the rate of longitudinal myocardial relaxation, is decreased (medial e ′ < 7 cm/s and lateral e ′ < 10 cm/s in). In constrictive pericarditis, e ′ velocity is relatively normal or even increased (Figs. 12-21 and 12-22), as increased lon- gitudinal motion of the heart, particularly medially, com- pensates for the loss of ventricular filling from constricted radial expansion of the heart. This longitudinal motion increases further as constriction worsens, with associated higher filling pressure, opposite to the change in e ′ with myocardial disease. This phenomenon has been termed annulus paradoxus (38), wherein E/e ′ is inversely propor- tional to pulmonary capillary wedge pressure, in contrast to myocardial disease, where E/e ′ increases with pulmonary capillary wedge pressure. However, in case of concomi- tant myocardial disease as in radiation injury or coronary artery disease, medial e ′ velocity may be less than 7 cm/s and annulus paradoxus may not apply (39). Furthermore, septal e ′ usually exceeds lateral mitral annulus e ′ , which is the reverse of the normal situation. This so-called “annulus reversus” (40) is observed in about 80% of patients with constriction (Fig. 12-22) (26,41) and occurs because the lateral annulus is tethered by adherent pericardium. It has
MAYO CLINIC DIAGNOSTIC CRITERIA FOR CONSTRICTION
Since there are several echocardiographic findings with constrictive pericarditis, we established a simple set of diagnostic criteria that can be used to identify constric- tion patients with high sensitivity and specificity (26). Five principal echocardiography parameters were tested in 166 patients (130) with surgically confirmed con- strictive and 36 with restrictive myocardial disease or severe tricuspid regurgitation who had a comprehensive
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