Constrictive pericarditis

 Typically occurs with TR…however, with severe valvular heart disease, there usually is
some myocardial disorder, and one would expect that there will be a decreased e’ which
is not the case with CP. Additionally, it is important to distinguish between the two,
since TR can mimic CP, but with the latter there will be expirational diastolic hepatic vein
flow reversal, rather than systolic which one sees in severe TR. Pericardiectomy causes
TR to get worse, so if pt is undergoing it, and has moderate or worse TR, then tricuspid
replacement or repair needs to be done.
 With myocardial disease, there will be hepatic vein inspiratory rather than expiratory
diastolic flow reversal. This is a good distinguisher from CP, because with myocardial
disease, inspiration leads to increased venous flow return to the heart, which the failing
RV cannot handle during diastole, and so leads to flow reversal from the increased
diastolic filling pressures.
 Ventricular interdependence can be seen in other conditions, such as COPD and asthma
(and tamponade and hyperventilation and obesity). However, in COPD and asthma,
there typically won’t be annulus reversus. The clincher is to look at SVC flow to the RA,
and with constriction, there is little inspiratory variation since the RA pressure is high,
but with COPD and asthma, inspiration will lead to a massive increase in flow to the
right heart.
 Kussmaul’s sign: inspiratory increase in JVP in CP (and also with some patients with
restrictive CM, so not specific for CP). Physiology is that with inspiration, it leads to an
increase in intra-abdominal pressure, and this leads to an increase in RAP. Typically if
RAP is normal, this is not a big deal, but with CP And RCM, the RAP increases so much
that there is very little flow from the SVC to the RA, and this is manifested with
increased JVP. (This will not happen with COPD as mentioned above)
