-TB earlier in the century, most common cause
-Now, most often idopathic, presumed 2o to idiopathic or viral pericarditis
-Stanford review of 95 pts who underwent pericardectomy ‘70-85:
Idiopathic 42%, S/p radiation 31% (majority from Hodgkins), S/p CT surgery ( mean time 35
months),Post infectious 6%, CTD ( RA, Lupus) 4%, Neoplasm 3%, Uremic 2%, Sarcoid 1%
->Kussmaul’s sign: absence of expected fall in JVP with inspiration. Seen due to failure of intrathoracic
pressure changes during respiration to be transmitted to the pericardial space and intracardiac chambers.
NOT sensitive for CP, can be see with many kinds of RHF ( restrictive, chronic RHF, etc). However, NOT
seen with tamponade.
(Pulsus paradoxus NOT seen usually, unless pericardial fluid present )
->Signs of RHF- edema, ascites, pulsatile hepatomegaly, effusions
->Knock 3rd heart sound, reportedly higher pitch and earlier than S3, caused by abrupt cessation in diastolic
filling. Coincides with rapid Y descent.
EKG: Nonspecific. Low volts sometimes. Afib occassionally
CXR: Shows calcs 50% of the time. One study of 135 pts showed only 27% with calcs. Also, calcified
pericaridium is not necessarily restrictive.
Echo: Thickening of pericardium. TEE better for measuring thickness of pericardium. Also abrupt post
]motion of ventricular septum in early diastole, due to rapid filling of compliant RV. Increased TV velocity
due to rapid early diastolic filling.
CT/MR: Both used to evaluate calcifications/ thickness. MRI considered most sensitive for measuring
Systolic function is normal
Diastole normal until size limit reached by ventricles-> filling abruptly stops ( accounts for dip/plateau)- in
contrast to tamponade where pressure are elevated throughout filling cycle
1) elevation and equalization of diastolic pressures (RVEDP increased ( usually 1/3 of RV
systolic pressure). LVEDP often higher than RVEDP i