Final The Echo Manual DIGITAL

The Echo Manual

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CHAPTER 12 PERICARDIAL DISEASES

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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