Introduction to clinical echocardiography: Pericardial disease, cardiomyopathies, and tumors





Objectives


On completion of this chapter, you should be able to:




  • Identify the echocardiographic distinction between pericardial effusion and pleural effusion



  • Describe the echocardiographic findings in cardiac tamponade



  • Describe the echocardiographic findings in dilated, restrictive, infiltrative, and hypertrophic cardiomyopathy



  • Recognize the echocardiographic findings of tumors, thrombus, vegetations, and normal variant





In addition to valvular heart disease, the sonographer may encounter fluid within the pericardial sac secondary to pericardial disease; enlargement of the cardiac chambers with regurgitant valvular flow as a result of dilated cardiomyopathy; increased thickness of the myocardium secondary to infiltrative cardiomyopathy; abnormal thickness of the interventricular septum compared with the posterior wall as seen in hypertrophic cardiomyopathy; or abnormal lesions within the cardiac chambers that represent tumors, thrombus, or vegetations. Each of these areas will be presented briefly to provide a basic understanding and investigative pathway for the sonographer.




Pericardial disease


The normal pericardium has two layers: the outer sac is the fibrous pericardium and the inner sac is the serous pericardium. The inner layer is further divided into the visceral layer (epicardium) that is continuous with the pericardial surface and covers the heart and proximal great vessels and the fibrous parietal layer ( Figure 34-1 ). The visceral layer is reflected to form the parietal epicardium. The visceral and parietal layers are separated by 15 to 50 ml of serous fluid. Their normal thickness is 1 to 2 mm and is abnormal if the thickness is greater than 4 mm.




FIGURE 34-1


​The pericardium consists of two layers: the fibrous outer layer and the inner double-layered sac known as the serous pericardium.


The pericardium has many functions. It provides a mechanical protection to the heart, provides a barrier to infection, reduces friction, and hemodynamically limits acute distention. The pericardial sac also contributes to the diastolic coupling and ventricular interdependence.


Pericardial effusion


The pericardial effusion is recognized as an echo-free space between the visceral and parietal pericardium. This fluid can be transudative, exudative, malignant, or hemorrhagic. The effusions first accumulate posterior to the heart and as the size increases extend laterally and then circumferentially.


Echocardiography is the primary method for the initial detection of pericardial effusion that occurs when fluid accumulates in the pericardial sac. This fluid usually accumulates posterior to the heart as this is the most dependent surface. As the effusion increases, it extends laterally and then may surround the apex and the anterior surface of the heart. It is important to distinguish the pericardial effusion from a possible pleural effusion. This is best imaged with transthoracic echocardiography (TTE) in the parasternal long-axis view with the deep image view. The round circle of the descending aorta may be seen posterior to the left atrium and serves as a landmark to distinguish pericardial from pleural effusion ( Figure 34-2 , A ). The pericardial effusion always is found anterior to the descending aorta, whereas the pleural effusion is posterior to the descending aorta ( Figure 34-2 , B ). Recall that the pericardium reflects off the aorta at this junction.




FIGURE 34-2


A, The round circle of the descending aorta (curved arrow) may be seen posterior to the left atrium and serves as a landmark to distinguish pericardial from pleural effusion. B, The pericardial effusion (straight arrow) always is found anterior to the descending aorta, whereas the pleural effusion is posterior to the descending aorta.


The estimation of the amount of fluid around the heart may be made with echocardiographic evaluation ( Table 34-1 ). The small effusions are the most obvious during systole. If the effusion is greater than 25 ml the echo-free space persists throughout the cardiac cycle. As the effusion increases in size, the parietal pericardium movement decreases. The small pericardial effusion would measure less than 0.5 cm in systole; a moderate effusion would measure 0.5 to 2.0 cm; and a large effusion would be over 2.0 cm ( Figure 34-3 ).



TABLE 34-1

Size of Pericardial Effusion
























Size Small Medium Large
Volume (ml) <100 100–500 >500
Localization Localized Circumferential Circumferential
Width (cm) <1 1–2 >2







FIGURE 34-3


A, The small pericardial effusion would measure less than 0.5 cm in systole; B, a moderate effusion would measure 0.5 to 2.0 cm; and C, a large effusion would be over 2.0 cm.


If there is only an echo-free space anterior to the right ventricle, the consideration of pericardial fat should be made ( Figure 34-4 ). If the patient has chronic effusions, fibrinous stranding within the fluid and on the epicardial surface of the heart may be noted ( Figure 34-5 ). Pericardial effusion with hemorrhage or purulent fluid is more heterogeneous and echogenic; such hemorrhagic effusions are more common in patients with metastatic disease. Loculated effusions may be seen in postsurgical patients.




FIGURE 34-4


If there is only an echo-free space anterior to the right ventricle, the consideration of pericardial fat should be made. AO, Aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.





FIGURE 34-5


A, If the patient has chronic effusions, fibrinous stranding within the fluid and on the epicardial surface of the heart may be noted. B, Pericardial effusion with hemorrhage or purulent fluid is more heterogeneous and echogenic. LV, Left ventricle; RV, right ventricle.


Cardiac tamponade


Cardiac tamponade occurs when the intrapericardial pressure increases to the point of compromising systemic venous return to the right atrium. The pressure and volume relationship is much stiffer when fluid accumulates rapidly. Echocardiographic findings are quite specific for tamponade: moderate to large pericardial effusion; right atrial systolic collapse; right ventricle diastolic collapse; reciprocal respiratory changes in ventricular volumes; and a dilated inferior vena cava with lack of respiratory changes ( Figure 34-6 ). Doppler findings will show a respiratory variation in the right ventricular (greater than 40% variation) and left ventricular (greater than 25% variation) diastolic filling ( Boxes 34-1 and 34-2 ). There is increased right ventricular filling on the first beat after inspiration and decreased left ventricular filling on the first beat after inspiration ( Figure 34-7 ).






FIGURE 34-6


A, PLA view of a patient with an acute moderate size pericardial effusion causing right ventricular collapse. B, M-mode tracing through the ventricles. C and D, Doppler of the mitral valve inflow shows respiratory variation. E, Subcostal image of the right heart diastolic collapse. F, M-mode demonstrates the diastolic collapse of the right ventricle (arrows). G, Subcostal view of the right atrial collapse. H, The inferior vena cava remained dilated, even with “sniffs.”


BOX 34-1

Cardiac Hemodynamics and Normal Respiratory Variation


With inspiration:





  • Intrathoracic pressure decreases, transmitted to all cardiac chambers → intrapericardial and intracardiac pressures decrease.



  • SVC and IVC are mostly extrathoracic and pressure remains relatively constant.



  • Pressure gradient between great veins and RA + RV increases → leading to ↑ right-sided heart filling. Tricuspid inflow varies by less than 25%.



  • ↑ in RV volume causes small compensatory ↓ in LV filling—”ventricular interdependence” (normal pulsus paradoxus less than 10 mm Hg).



  • Pulmonary veins and LA + LV are entirely intrathoracic and have an almost equal decrease in pressures, hence overall pressure gradient between PV and LV remains constant with little change in LV filling through the respiratory cycle. Mitral inflow varies by less than 15%.



With expiration:





  • Intrathoracic, intrapericardial, and intracardiac pressures ↑, with a mild decrease in RV filling and a subsequent increase in LV filling.



IVC, Inferior vena cava; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; SVC, superior vena cava.



BOX 34-2

Cardiac Hemodynamics and Respiratory Variation in Tamponade


With inspiration:





  • On right side, ↓ in intrathoracic pressure is transmitted to intrapericardial space and both pericardial and intracardiac pressures ↓ relative to SVC/IVC pressures → RV filling increases.



  • Tricuspid inflow varies greater than 25% with respiration.



  • Ventricular interdependence makes septum bow toward LV to accommodate ↑ RV volume, leading to ↓ LV filling.



  • On left side, there is a ↓ in intrathoracic and PV (PCWP) pressures but only a small ↓ in intrapericardial and intracardiac pressures. So, LV filling gradient decreases leading to decreased LV filling.



  • Decreased LV filling allows for increased RV filling (ventricular interdependence).



  • Mitral inflow varies greater than 15%.



With expiration:





  • RV filling is decreased slightly and LV filling is restored.



IVC, Inferior vena cava; LV, left ventricle; PCWP, pulmonary capillary wedge pressure; PV, pulmonary vein; RV, right ventricle; SVC, superior vena cava.




FIGURE 34-7


A, Left ventricle filling with inspiration (normal). Changes in intrathoracic pressure are transmitted equally to the pericardial sac and pulmonary veins. The effective filling gradient (EFG) changes only slightly with respiration. B, Left ventricle filling with inspiration (tamponade). Changes in intrathoracic pressure are transmitted to the pulmonary veins but not to the pericardial sac; the EFG falls during inspiration.


Constrictive pericarditis


In chronic pericardial disease the pericardium may become thickened and inelastic, which in turn limits the ventricular filling, leading to chronic biventricular diastolic dysfunction, right-sided heart failure, and low systemic output. This condition is secondary to long-standing pericardial inflammation with pericardial scarring, thickening, fibrosis, and calcification. Causes of constriction include prior cardiac surgery, acute or chronic/recurrent pericarditis, mediastinal radiation, tuberculous pericarditis, trauma, or idiopathic.


On echocardiography there may be thickening of the pericardial layer with increased echogenicity ( Figure 34-8 ). There may be normal left ventricular size and systolic function. There is biatrial enlargement. The septum is quite abnormal: there may be an abrupt posterior motion of the ventricular septum in early diastole, a flat motion in middle diastole, an abrupt anterior motion following atrial contraction, or a septal “bounce” demonstrating an exaggerated interventricular dependence. The left ventricular posterior wall may be abnormal with a rapid movement during diastole, then flat during mid to late diastole, with an abrupt termination of ventricular filling. The inferior vena cava is dilated with minimal respiratory variation.






FIGURE 34-8


A, Gross specimen of the thickened pericardial layers as seen in pericardial constriction. B, On radiography, the pericardium appears densely calcified. C, Subcostal image demonstrates a thickened pericardial layer (arrow). D, Doppler evaluation of the mitral valve demonstrates increased early diastolic filling velocity followed by rapid deceleration, leading to a short filling time.


Doppler findings in constrictive pericarditis reflect abnormal hemodynamics ( Box 34-3 ). The mitral inflow pattern demonstrates increased early diastolic filling velocity followed by rapid deceleration, leading to a short filling time. There may be dynamic changes with respiration: early diastolic mitral inflow is reduced with the onset of inspiration, and the isovolumic relaxation time shortens and returns to normal with expiration. The pulmonary venous flow may show respiratory changes. The systolic wave and early diastolic wave velocities are increased during expiration and decreased during inspiration. The diastolic flow reversal is augmented in expiration in the hepatic vein flow. There may be a prominent “y” descent on the hepatic vein or superior vena cava flow pattern.



BOX 34-3

Constrictive Pericarditis

































Echocardiogram Finding
Right atrial pressure
RV/LV filling pressures ↑ RV = LV
Pulmonary artery pressures Mild
RV diastolic pressure plateau Greater than one-third peak RV pressure
Diastolic filling Rapid, early, impaired late
2D echocardiography Pericardial thickening without effusion
Doppler E > a on LV inflow
Prominent “y” descent in hepatic vein
Prom “a” wave in pulmonary valve flow
Respiratory variation in IVRT, E velocity
Other diagnostic testing CT or MRI for pericardial thickening


CT, Computed tomography; IVRT, isovolumic relaxation time; LV, left ventricle; MRI, magnetic resonance imaging; RV, right ventricle.





Cardiomyopathies


Cardiomyopathy may be defined as a primary myocardial disorder that is not related to the effects of valvular heart disease, hypertension, or coronary artery disease. Traditionally cardiomyopathies may be divided into these categories: dilated/congestive, restrictive/infiltrative, arrhythmogenic right ventricular dysplasia, hypertrophic, and unclassified (e.g., endomyocardial fibroelastosis). This section will focus on dilated, restrictive, and hypertrophic cardiomyopathies. Echocardiography plays a primary role in the assessment of the patient with congestive heart failure and suspected cardiomyopathy. The echocardiographic study not only provides prognostic information, but serves as a guide to the success of therapy.


Dilated/congestive cardiomyopathy


Dilated cardiomyopathy is characterized by the dilation and reduced contractility of the left ventricle or both the left and right ventricles. There are multiple causes of dilated cardiomyopathy, as noted in Box 34-4 . The abnormalities that may be seen with two-dimensional (2D) echocardiography include the following:


May 29, 2019 | Posted by in ULTRASONOGRAPHY | Comments Off on Introduction to clinical echocardiography: Pericardial disease, cardiomyopathies, and tumors
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