(BQ) Part 2 book Textbook of clinical echocardiography presents the following contents: Pericardial disease, valvular stenosis, valvular regurgitation, prosthetic valves, endocarditis, cardiac masses and potential cardiac source of embolus, diseases of the great arteries, the adult with congenital heart disease, intraoperative and interventional echocardiography.
10 Pericardial Disease PERICARDIAL ANATOMY AND PHYSIOLOGY PERICARDITIS Basic Principles Echocardiographic Approach Clinical Utility PERICARDIAL EFFUSION Basic Principles Diagnosis of Pericardial Effusion Diffuse Effusion Loculated Effusion Distinguishing from Pleural Fluid Clinical Utility PERICARDIAL TAMPONADE Echocardiographic Approach Right Atrial Systolic Collapse Right Ventricular Diastolic Collapse PERICARDIAL ANATOMY AND PHYSIOLOGY The pericardium consists of two serous surfaces surrounding a closed, complex, saclike potential space The visceral pericardium is continuous with the epicardial surface of the heart The parietal pericardium is a dense but thin fibrous structure that is apposed to the pleural surfaces laterally and blends with the central tendon of the diaphragm inferiorly Around the right and left ventricles (RV and LV) and the ventricular apex, the pericardial space is a simple ellipsoid structure conforming to the shape of the ventricles Around the systemic and pulmonary venous inflows and around the great vessels, the parietal and visceral pericardia meet to close the “ends” of the sac—these areas often are referred to as pericardial reflections The pericardial space encloses the right atrium (RA) and RA appendage anteriorly and laterally, with pericardial reflections around the superior and inferior vena cavae near their junction with the RA Superiorly, the pericardium extends a short distance along the great vessels, with a small “pocket” of pericardium surrounding the great arteries posteriorly—the transverse sinus The pericardial space extends laterally to the left atrium (LA), and a blind pocket of the pericardium 254 Reciprocal Changes in Ventricular Volumes Respiratory Variation in Diastolic Filling Tissue Doppler Early-Diastolic Velocity Inferior Vena Cava Dilation Clinical Utility Diagnosis of Pericardial Tamponade Echo-Guided Pericardiocentesis PERICARDIAL CONSTRICTION Basic Principles Echocardiographic Approach Imaging Doppler Examination Constrictive Pericarditis versus Restrictive Cardiomyopathy Clinical Utility SUGGESTED READING extends posteriorly to the LA, between the four pulmonary veins—the oblique sinus (Fig 10-1) The pericardial space normally contains a small amount (5 to 10 mL) of fluid that may be detectable by echocardiography Anatomically, the pericardium isolates the heart from the rest of the mediastinum and from the lungs and pleural space, serving as a barrier to infection and reducing friction with surrounding structures during contraction, rotation, and translation of the heart In addition, the semirigid enclosure provided by the pericardium affects the pressure distribution to the cardiac chambers and mediates the interaction between RV and LV diastolic filling The importance of the pericardium is most evident when affected by disease processes such as inflammation, thickening or fluid accumulation PERICARDITIS Basic Principles Pericarditis is inflammation of the pericardium, and it can be due to a wide variety of causes, including bacterial or viral infection, trauma, uremia, and transmural myocardial infarction (Table 10-1) Clinically, the Pericardial Disease | Chapter 10 Superior vena cava R pulmonary a Arch of aorta L pulmonary a Cut pericardial sleeve: Around arteries Around veins R superior and inferior pulmonary vv Ascending aorta Pulmonary trunk L superior and inferior pulmonary vv Cut edge of fibrous pericardium TABLE 10-1 Causes of Pericardial Disease (with Examples) Idiopathic Infections Viral Bacterial (Staphylococcus, pneumococcus, tuberculosis) Parasitic (Echinococcus, amebiasis, toxoplasmosis) Malignant Metastatic disease (e.g., lymphoma, melanoma) Direct extension (e.g., lung carcinoma, breast carcinoma) Primary cardiac malignancy Inflammatory Figure 10–1 Pericardial anatomy The posterior wall of the pericardial sac after the heart has been removed by severing its continuity with the great arteries and veins and by cutting the two pericardial sleeves that surround the arteries and veins The parietal serous pericardium is dark red, the fibrous pericardium is pink, the horizontal arrow is in the transverse sinus, and the vertical arrow is in the oblique sinus of the pericardium. (Reprinted with permission from Rosse C, Goddum-Rosse P: Hollinshead’s Textbook of Anatomy, 5th ed Philadelphia: Lippincott-Raven, 1997.) diagnosis of pericarditis is based on at least two of the four characteristic features: Post-myocardial–infarction (e.g., Dressler’s syndrome) Uremia Systemic inflammatory diseases (e.g., lupus, scleroderma) Post-cardiac surgery Radiation Intracardiac-Pericardial Communications Blunt or penetrating chest trauma Postcatheter procedures Postinfarction LV rupture Aortic dissection n n n n ypical chest pain T Widespread ST elevation or PR depression on ECG Pericardial rub on auscultation New or increasing pericardial effusion While it is probable that most patients with pericarditis have a pericardial effusion at some point in the disease course, a pericardial effusion is not a necessary criterion for a diagnosis of pericarditis, nor does the presence of an effusion indicate a diagnosis of pericarditis Interestingly, there is no correlation between the size of the pericardial effusion and the presence or absence of a pericardial “rub” on physical examination Echocardiographic Approach In a patient with suspected pericarditis, the echocardiogram may show a pericardial effusion of any size, pericardial thickening with or without an effusion, or it may be entirely normal A pericardial effusion is recognized as an echolucent space around the heart (Fig 10-2) Pericardial thickening is evidenced by increased echogenicity of the pericardium on two-dimensional (2D) imaging and as multiple parallel reflections posterior to the LV on M-mode recordings (Fig 10-3) However, because the pericardium typically is the most echogenic structure in the image, it can be difficult to distinguish normal from thickened pericardium, and other imaging approaches, such as computed tomography (CT) or magnetic resonance (CMR), are more sensitive for this diagnosis Examination from several windows is needed when pericarditis is suspected, because effusion or thickening can be localized and may be seen in only certain tomographic views If a pericardial effusion is present, the possibility of tamponade physiology should be considered If pericardial thickening is present, examination for evidence of constrictive physiology should be considered Clinical Utility Pericarditis is a clinical diagnosis that cannot be made independently by echocardiography The goal of the echocardiographic examination is to evaluate for pericardial effusion or thickening and to evaluate for tamponade physiology PERICARDIAL EFFUSION Basic Principles A wide variety of disease processes can result in a pericardial effusion with a differential diagnosis similar to that for pericarditis (see Table 10-1) The physiologic consequences of fluid in the pericardial space depend 255 256 Chapter 10 | Pericardial Disease PE RV RV Ao LV LA PE PE DA B A Figure 10–2 Pericardial effusion on echocardiography Parasternal long- and short-axis views of a moderate circumferential pericardial effusion (PE) In the long-axis view (A) and short-axis view (B), the effusion tracks appear anterior to the descending aorta (DA) with a small amount of fluid posterior to the LA in the oblique sinus Pericardial fluid in the transverse sinus (posterior to the aorta [Ao]) delineates the right pulmonary artery (arrow) which is not usually seen in this view in adults Pericardial fluid anterior to the RV is seen in both the long- and short-axis views LV Figure 10–3 Pericardial thickening on M-mode echocardiography Multiple parallel dense echos (arrow) are seen posterior to the LV epicardium This patient also has a small pericardial effusion (PE), seen on M-mode as an echo-free space between the flat pericardium and moving posterior wall both on the volume and rate of fluid accumulation A slowly expanding pericardial effusion can become quite large (>1000 mL) with little increase in pericardial pressure, whereas rapid accumulation of even a small volume of fluid (50 to 100 mL) can lead to a marked increase in pericardial pressure (Fig 10-4) Tamponade physiology occurs when the pressure in the pericardium exceeds the pressure in the cardiac chambers, resulting in impaired cardiac filling (Fig 10-5) As pericardial pressure increases, filling of each cardiac chamber is sequentially impaired, with lower-pressure chambers (atria) affected before higher-pressure chambers (ventricles) The compressive effect of the pericardial fluid is seen most clearly in the phase of the cardiac cycle when pressure is lowest in that chamber—systole for the atrium, diastole for the ventricles Filling pressures become elevated as a compensatory mechanism to maintain cardiac output In fully developed tamponade, diastolic pressures in all four cardiac chambers are equal (and elevated) because of exposure of the entire heart to the elevated pericardial pressure Clinically, tamponade physiology manifests as lowcardiac output symptoms, hypotension, and tachycardia Jugular venous pressure is elevated and pulsus paradoxus (an inspiratory decline >10 mm Hg in systemic blood pressure) is present on physical examination The clinical finding of pulsus paradoxus is closely related to the echo findings of reciprocal respiratory changes in RV and LV filling and emptying Pericardial pressure (mm Hg) Pericardial Disease | Chapter 10 20 10 0 50 100 150 200 Pericardial volume (mL) CO MAP Pressure (mm Hg) 100 PP RAP 50 RA RV PP RAP Cardiac output (L/min) Figure 10–4 Pericardial pressure versus pericardial volume The graph shows an acute effusion (blue line, with a steep pressure-volume relationship) and a chronic effusion (yellow line, where large volumes may lead to only mild pressure elevation) 0 50 100 150 200 Pericardial volume (mL) Figure 10–5 Relationship among pericardial pressure (PP), RA pressure (RAP), mean arterial pressure (MAP), and cardiac output (CO) Note that when pericardial pressure exceeds RA pressure, blood pressure and cardiac output fall When RV pressure is exceeded (at the arrow), cardiac output and mean arterial pressure fall further Diagnosis of Pericardial Effusion The sensitivity and specificity of echocardiography for detection of a pericardial effusion are very high Diagnosis continues to rely on 2D transthoracic echocardiographic (TTE) imaging from multiple acoustic windows; transesophageal echocardiography (TEE) sometimes may be helpful with loculated posterior effusions Three-dimensional (3D) imaging is not needed routinely but may be helpful in the diagnosis of loculated effusions or hematomas Diffuse Effusion A pericardial effusion is recognized as an echolucent space adjacent to the cardiac structures In the absence of prior pericardial disease or surgery, pericardial effusions usually are diffuse and symmetric with clear separation between the parietal and visceral pericardium (Fig 10-6) A relatively echogenic area anteriorly, in the absence of a posterior effusion, most likely represents a pericardial fat pad M-mode recordings are helpful, especially with a small effusion, showing the flat posterior pericardial echo reflection and the moving epicardial echo with separation between the two in both systole and diastole In the apical views, the lateral, medial, and apical extent of the effusion can be appreciated In the apical four-chamber view, an isolated echo-free space superior to the RA most likely represents pleural fluid The subcostal view demonstrates fluid between the diaphragm and RV and is particularly helpful in echoguided pericardiocentesis The size of the pericardial effusion is considered to be small when the separation between the heart and the parietal pericardium is 2 cm More quantitative measures of the size of the pericardial effusion rarely are needed in the clinical setting In patients with recurrent or long-standing pericardial disease, fibrinous stranding within the fluid and on the epicardial surface of the heart may be seen When a malignant effusion is suspected, it is difficult to distinguish this nonspecific finding from metastatic disease Features suggesting the latter include a nodular appearance, evidence of extension into the myocardium, and the appropriate clinical setting (Fig 10-7) Loculated Effusion After surgical or percutaneous procedures, or in patients with recurrent pericardial disease, pericardial fluid may be loculated (Fig 10-8) In this situation, the effusion is localized by adhesions to a small area of the pericardial space or consists of several separate areas of pericardial effusion, separated by adhesions Recognition of a loculated effusion is especially important because hemodynamic compromise can occur with even a small, strategically located fluid collection In addition, drainage of a loculated effusion may not be possible from a percutaneous approach Distinguishing from Pleural Fluid In order to reliably exclude the possibility of a loculated pericardial effusion, echocardiographic evaluation requires examination from multiple acoustic windows The parasternal approach demonstrates the extent of the fluid collection at the base of the heart in both long- and short-axis views Note that pericardial fluid may be seen posterior to the LA (in the oblique sinus), as well as posterior to the LV Care should be taken that the coronary sinus or descending thoracic aorta is not mistaken for pericardial fluid In fact, these structures can help in distinguishing pericardial from pleural fluid, because a left pleural effusion will extend posterolaterally to the descending aorta, 257 258 Chapter 10 | Pericardial Disease Figure 10–6 Circumferential pericardial effusion The echolucent effusion (PE) is seen in parasternal longaxis, short-axis, apical four-chamber, and subcostal views in a patient early after mechanical aortic valve replacement Note the shadowing and reverberations from the valve in the parasternal long-axis view LV LV LA PE PE PE RV RV RA LV LV LA RA LA Pleural fluid Hematoma PE Lung RV RV LV LV RA LA Figure 10–7 Malignant pericardial effusion Apical four-chamber view in a patient with metastatic lymphoma shows a small pericardial effusion (PE) in the apical region with marked thickening and irregularity of the pericardium (cyan arrows), suggesting tumor involvement Pleural fluid with compressed lung also is evident The small fluid collection adjacent to the LA (yellow arrow) may be pericardial fluid in the oblique sinus of the pericardium Figure 10–8 Pericardial hematoma TEE transgastric short-axis view in a patient with acute hypotension during an electrophysiology procedure shows a localized hematoma in the pericardial space with compression of the RV The catheter in the RV (cyan arrow) casts a dark shadow that obscures part of the ventricular septum whereas a pericardial effusion will track anterior to the descending aorta (Fig 10-9) When a large left pleural effusion is present, sometimes cardiac images can be obtained with the transducer on the patient’s back (Fig 10-10) Pericardial Disease | Chapter 10 APICAL VIEW Ao LV LA LV LA CS DA Pericardial DA RV RA Pleural Figure 10–9 Pericardial versus pleural fluid Schematic diagram of the relationship between a pericardial effusion and the descending aorta (DA) compared with a left pleural effusion Pericardial fluid tracks posterior to the LA in the oblique sinus of the pericardium, anterior to the descending aorta Ao, aorta; CS, coronary sinus PT sitting scanning from back Pleural fluid Clinical Utility Echocardiography is very sensitive for the diagnosis of pericardial effusion, even when loculated, if care is taken to examine the heart in multiple tomographic planes from multiple acoustic windows Loculated effusions can be difficult to assess in certain locations, particularly if localized to the atrial region, because the effusion itself may be mistaken for a normal cardiac chamber TEE imaging may better detect and define the extent of loculated effusions after cardiac surgery, especially when located posteriorly (Fig 10-11) Pericardial adipose tissue is common, especially anterior to the RV, and it may be mistaken for an effusion Unlike pericardial fluid, adipose tissue exhibits a fine pattern of echogenicity, which helps with identification of this normal finding A pericardial cyst is an uncommon congenital fluid filled sac, usually adjacent to the right heart Pericardial cysts may be missed on echocardiography and are better evaluated by chest CT or CMR However, when present, they may be mistaken for a pericardial or pleural effusion The cause of the pericardial effusion is not always evident on echocardiographic examination Irregular pericardial or epicardial masses in a patient with a known malignancy certainly raise the possibility of a malignant effusion, but this appearance can be mimicked by a fibrinous organization of a long-standing pericardial effusion Masses adjacent to the cardiac structures (in the mediastinum) resulting in pericardial effusion can be missed by echocardiography Wideview tomographic imaging procedures, such as CT or CMR, are helpful in these cases Obviously, whether a pericardial effusion is infected or inflammatory in etiology cannot be determined by DA LA LV Ao Figure 10–10 Large pleural effusion In a view with the transducer moved laterally from the apical position (top), a large left pleural effusion is seen This can be distinguished from pericardial fluid by the position of the descending aorta (DA), the presence of compressed lung, and by identification of both layers of the pericardium adjacent to the myocardium Images also were obtained with the transducer on the patient’s back (bottom), demonstrating the relationship between the pleural fluid and the descending aorta echocardiography Depending on the associated clinical findings in each case, diagnostic pericardiocentesis, pericardial biopsy, or both may be indicated to establish the correct diagnosis With pericardial effusion due to aortic dissection or cardiac rupture (either as a consequence of myocardial infarction or a procedure) the entry site into the pericardium rarely can be detected, so a high level of suspicion is needed when these diagnoses are a possibility The site of an LV rupture may be “contained” by pericardial adhesions, resulting in formation of a pseudoaneurysm A pseudoaneurysm is defined as a saccular structure communicating with the ventricle with walls composed of pericardium In contrast, the walls of a “true” aneurysm are composed of thinned, scarred myocardium (see Fig 8-27) 259 260 Chapter 10 | Pericardial Disease LA RV LV Respiratory “paradoxic” septal motion Systole LA RA collapse Pericardial effusion LV RV collapse Figure 10–11 TEE imaging of pericardial hematoma TTE imaging was nondiagnostic because of poor ultrasound tissue penetration in this patient with a recently implanted LV assist device and low cardiac output This TEE four-chamber view shows a hematoma around the LV apex (arrows), which was compressing the RV and obstructing flow into the LV assist device The right heart catheter (small arrow) casts a shadow over the hematoma Diastole RA LA Figure 10–12 2D echo findings with tamponade physiology PERICARDIAL TAMPONADE Right Ventricular Diastolic Collapse Echocardiographic Approach RV diastolic collapse occurs when intrapericardial pressure exceeds RV diastolic pressure and when the RV free wall is normal in thickness and compliance The presence of RV hypertrophy or infiltrative diseases of the myocardium may allow development of a pressure gradient between the pericardial space and the RV chamber without inversion of the normal contour of the free wall RV diastolic collapse is best appreciated in the parasternal long-axis view or from a subcostal window If the timing of RV wall motion is not clear on 2D imaging, an M-mode recording through the RV free wall is helpful The presence of RV diastolic collapse is somewhat less sensitive (60% to 90%) but more specific (85% to 100%) than brief RA systolic collapse for diagnosing tamponade physiology (Fig 10-14) When cardiac tamponade occurs with a diffuse, moderate to large pericardial effusion, the associated physiologic changes are evident on echocardiographic and Doppler examination (Fig 10-12), including: n n n n n n A systolic collapse >1⁄3 systole R RV diastolic collapse Reciprocal respiratory changes in RV and LV volumes (septal shifting) Reciprocal respiratory changes (>25%) in RV and LV filling Reduced early-diastolic tissue Doppler velocity Severe dilation of the inferior vena cava Right Atrial Systolic Collapse Reciprocal Changes in Ventricular Volumes When intrapericardial pressure exceeds RA systolic pressure (lowest point of the atrial pressure curve), inversion or collapse of the RA free wall occurs Because the RA free wall is a thin, flexible structure, brief RA wall inversion can occur in the absence of tamponade physiology However, the longer the duration of RA inversion relative to the cycle length, the greater is the likelihood of cardiac tamponade Inversion for greater than a third of systole has a sensitivity of 94% and a specificity of 100% for the diagnosis of tamponade Careful frame-by-frame 2D-image analysis is needed for this evaluation (Fig 10-13) Reciprocal respiratory variation in RV and LV volumes, and consequent septal shifting, may be seen on 2D imaging when tamponade is present In the apical fourchamber view, an increase in RV volume with inspiration (shift in septal motion toward the LV in diastole and toward the RV in systole) and a decrease during expiration (normalization of septal motion) can be appreciated This pattern of motion corresponds to the physical finding of pulsus paradoxus The proposed explanation for this observation is that total pericardial volume (heart chambers plus pericardial fluid) is fixed in tamponade; thus as intrathoracic pressure becomes more negative Pericardial Disease | Chapter 10 RV LV LV RA LA PE LA PE Figure 10–14 RV diastolic collapse Apical four-chamber view with a large pericardial effusion (PE) and tamponade physiology resulting in the compression (or collapse) of the RV (arrows) and the RA in diastole Figure 10–13 RA systolic collapse Apical four-chamber view showing systolic collapse on the RA free wall (arrow) in a patient with clinical tamponade physiology PE, pericardial effusion during inspiration, enhanced RV filling limits LV diastolic filling This pattern reverses during expiration Respiratory Variation in Diastolic Filling Doppler recordings of RV and LV diastolic filling in patients with tamponade physiology show a pattern that parallels the changes in ventricular volumes With inspiration, the RV early-diastolic filling velocity is augmented, while LV diastolic filling diminishes (Figs 10-15 and 10-16) In addition, the flow velocity integral in the pulmonary artery increases with inspiration, while the aortic flow velocity integral decreases In the acutely ill patient, these changes can be difficult to demonstrate in part because of respiratory changes in the intercept angle between the Doppler beam and the flow of interest, causing artifactual apparent velocity changes Differentiating the normal respiratory variation in diastolic filling from the excessive variation (>25%) seen in tamponade may be subtle in borderline cases Tamponade physiology is not an all-or-none phenomenon; a patient may exhibit varying degrees of hemodynamic impairment as the degree of pericardial compression (pericardial pressure) increases Tissue Doppler Early-Diastolic Velocity The early-diastolic mitral annular tissue Doppler velocity (E′) is reduced when tamponade is present and returns to normal after pericardiocentesis, likely reflecting changes in cardiac output However, respiratory variation is not seen and the sensitivity and specificity of this finding have not been evaluated Inferior Vena Cava Dilation Inferior vena cava plethora, a dilated inferior vena cava with