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posted Jul 16, 2014, 4:25 AM by Joshua Sabari   [ updated Jul 16, 2014, 6:28 AM ]
Jonathan Ross PGY-3 



This week’s CRS conference addressed the case of a 65-year old man with “cryptogenic cirrhosis” who presented with worsening lower extremity edema and ascites. Interestingly, he had elevated JVP, no stigmata of liver disease, and normal liver tests, which pointed us toward a cardiac etiology of his ascites. We followed along as an extensive battery of tests ultimately led to a diagnosis of constrictive pericarditis. For this Monte Minute I’ll look at some clinical characteristics of chronic constrictive pericarditis.


Chronic constrictive pericarditis results from the healing process (a fibrinous process leading to formation of granulation tissue and scarring of the pericardium) after an inflammatory event, including acute or relapsing viral pericarditis, bacterial pericarditis (much rarer), other infection (TB in much of the world), trauma, cardiac surgery, irradiation, neoplastic disease, autoimmune disease, or uremia.


Here is the breakdown from a 2004 case series describing 163 patients who underwent pericardiectomy with confirmed constrictive pericarditis.

- idiopathic or viral in 75 patients (46%)

- postsurgical in 60 patients (37%)

- secondary to prior mediastinal irradiation in 15 patients (9%)

-  miscellaneous in 13 patients (8%) – including TB, rheumatoid arthritis, SLE, prior trauma, Wegener’s granulomatosis and purulent pericarditis


Unlike the normal pericardium which allows the heart to take in the increased venous return during inspiration, the thickened/scarred pericardium does not allow normal cardiac expansion. The ventricles fill normally during early diastole but then can’t fully expand. Think about a heart in a box.  For you physical exam junkies / Jerry Paccione disciples, this rapid early diastolic filling can be seen as a prominent y descent of the JVP wave when you’re looking at the neck veins.  As the pericardium becomes thicker and more constrictive, chamber pressures equalize as the ventricles fill and stroke volume and cardiac output are reduced.



This is often an indolent process. Symptoms may include fatigue, weight gain, increased abdominal girth, lower extremity edema, dyspnea on exertion. There may be a history of acute pericarditis (i.e. pleuritic, positional chest pain +/- fever). On exam jugular veins are distended (and may stay up on inspiration…Kussmaul’s sign!).  As mentioned above there may be a prominent y descent of the JVP. Other possible cardiac findings include distant heart sounds, decreased apical impulse and a pericardial knock. Moving down you might note a pulsatile liver, ascities and even jaundice if there is significant congestion in the liver. LE edema is common. As we saw in the CRS case, the paradoxical presentation of ascites with elevated JVP is an important clue to consider.


Not satisfied with just the history and exam? Here are a few other modalities that may help you:

- EKG – can see low voltage secondary to the thickened pericardium. Acute pericarditis classically has PR-segment depression and diffuse STE, though these are often not present in the more chronic process of constrictive pericarditis

- Echo – usually (though not always, as we saw in today’s case) can confirm the diagnosis of constrictive pericarditis. Specific findings to look for include pericardial thickening, dilation of IVC/hepatic veins, and (on Doppler) a rapid stopping of ventricular filling in early diastole (when the pericardium maxes out). There may be ‘bowing’ of the septum into the LV during inspiration (since the RV can’t expand outward) and in the opposite direction during expiration (as the LV pushes it to the right).

- CXR – may see calcification of the pericardium

- MRI or CT – these are more sensitive for a thickened pericardium

- cardiac cath +/- endomyocardial biopsy can be used to confirm pericardial disease and exclude restrictive CM


Note – though not mentioned above, it is also important to work up potential etiologies of the process that ultimately led to the constrictive pericarditis, i.e. TB, autoimmune disease, etc., if clinical suspicion for any of these exists.


In a word, surgery (pericardiectomy). In less severe cases diuretics can help relieve symptoms associated with fluid overload. For severe ascities therapeutic paracentesis is often indicated.


It’s often difficult to differentiate these two processes since they may present very similarly both in terms of symptomatology and hemodynamics. This table from Harrison’s sums it up pretty nicely though: (see word document file). 

For a more in-depth look at constrictive pericarditis, check out the Lancet review



Troughton RW, et al, Pericarditis. Lancet. 2004;363(9410).

Harrison’s, Chap. 239 – Pericardial disease

Bertog, et al, J Am Coll Cardiol. 2004;43(8)

Joshua Sabari,
Jul 16, 2014, 6:28 AM
Joshua Sabari,
Jul 16, 2014, 4:25 AM