Overview of Echocardiographic Assessment of Pericardial Disease

The pericardium is a double-layered structure consisting of a fibrous outer layer and an inner serous layer with visceral and parietal components. The space between these layers normally contains less than 50 ml of fluid, acting as a lubricant. The pericardium provides mechanical protection, limits cardiac chamber distension, facilitates ventricular coupling, and has anti-inflammatory functions. Its thickness, measured by CT and CMR, varies, and it's not essential for life but performs vital functions.

Pericarditis is inflammation of the pericardium, with common causes being viral infection and idiopathic. Echo is the first-line imaging assessment due to its low cost and wide availability. While acute pericarditis can present with a normal echo in 40-50% of cases, findings can include increased pericardial brightness/thickening, abnormal septal balance (suggesting early constriction), intra-pericardial fibristands, intra-pericardial masses, and pericardial effusion (from trivial to large). Echo also helps differentiate pericarditis from myocardial ischemia.

While echo is primary, CT with contrast is useful for identifying etiology, assessing calcifications (especially before pericardiectomy), and evaluating anatomy. CMR can differentiate myocardial tissue, visualize inflammation, and assess fibrosis patterns. These are useful if echo is inconclusive, treatment fails, or atypical presentations or suspicion of malignancy/infection arise. ESC guidelines give Class I indications for CT for thickness, calcification, and masses, and for CMR for edema and late gadolinium enhancement.

Pericardial effusion is fluid accumulation in the pericardial space. Effusion size (small, moderate, large, very large) does not directly correlate with its physiological effects. Rapid effusions cause a steep rise in pericardial pressure leading to tamponade physiology quickly, even with small volumes. Slow-growing effusions allow more time for pericardial stretch, accommodating larger volumes. Ventricular interdependence, where filling of one chamber impacts the other, is key to understanding tamponade. Inspiration increases venous return to the RV, shifting the septum towards the LV, and vice versa during expiration.

Tamponade is a life-threatening condition caused by cardiac chamber compression, leading to reduced cardiac output. It's fundamentally a clinical diagnosis. Echo signs include RA collapse (duration exceeding one-third of the cardiac cycle is highly specific), early diastolic RV collapse (worse during expiration), and a 'swinging heart' phenomenon. Doppler findings crucial for tamponade include a >25% (or 30% by ASE) inspiratory reduction in mitral E-wave velocity, and a >40% inspiratory increase in tricuspid E-wave velocity. LVOT respiratory variation (a >10% drop with inspiration) and IVC plethora (dilated, non-collapsible IVC) are also important signs, though IVC plethora is highly sensitive but not specific.

Atypical tamponade presentations include low-pressure tamponade (low pericardial pressures despite compression, often due to acute volume loss or rapid fluid accumulation), tamponade with pulmonary hypertension (absence of RV/RA collapse due to already high right-sided pressures), and localized effusions (post-cardiac surgery, where clinical findings depend on effusion location). Volume resuscitation is crucial for low-pressure tamponade.

Constrictive pericarditis involves a thickened, scarred, inelastic, and often calcified pericardium that limits diastolic ventricular filling. Causes include viral pericarditis, cardiac surgery, radiation, and idiopathic. Cardiac surgery is now the most common known cause in developed countries. Diagnosis is multimodal, with echo, right heart cath, and CT imaging. Notably, normal pericardial thickness does not rule out constriction, as it's the stiffness, not just thickness, that causes the phenomenon. Claude Beck's chronic cardiac compression triad (high venous pressure, small quiet heart, ascites) describes chronic constriction.

The stiff pericardium prevents intrathoracic pressure changes from influencing cardiac chambers. Inspiration leads to RV filling at the expense of LV, and vice versa during expiration, causing significant respiratory variation in the septal motion. Right-sided flow velocities increase with inspiration, and left-sided with expiration. A key differentiating sign is 'annulus reversus', where lateral E' is lower than medial E' on tissue Doppler, indicating tethering of free walls while septal wall motion is preserved. The Mayo Clinic criteria for constrictive pericarditis combines IVC plethora, mitral E/A ratio, septal shift, annulus reversus, and hepatic vein diastolic reversal.

Constrictive pericarditis is a pericardial disease with normal myocardium, while restrictive cardiomyopathy is a myocardial disease with normal pericardium. Tissue Doppler is crucial for differentiation: restriction shows low tissue Dopplers overall due to stiff myocardium, while constriction (where myocardium is normal) shows enhanced tissue Dopplers longitudinally, particularly in the medial E' (annulus reversus), as the heart can only move in this direction due to the stiff pericardium. Other uncommon pericardial syndromes include effusive-constrictive pericarditis, defined by persistent elevated intracardiac pressures post-pericardiocentesis for tamponade.