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What do we have here? A nice case, poll (below) in thread, and explanation to follow for all the #EchoFirst enthusiasts. #FellowsFirst #ACCFIT #cardiotwitter #ASE360
What do you think is the mechanism for these 2D and Doppler findings? @DavidWienerMD @iamritu @purviparwani @ErinMichos @DrMarthaGulati @HeartDocSharon @HeartOTXHeartMD @mmamas1973 @onco_cardiology @kgzimmerman @rajdoc2005 @DocStrom
1/ 
There is constriction, but specifically effusive-constrictive pericarditis.
#tweetorial here:
To understand #EchoFirst findings in pericardial disease, must go back to basics
Remember that superior portion of LA and pulmonary veins are extra-pericardial structures.
There is constriction, but specifically effusive-constrictive pericarditis. #tweetorial here: To understand #EchoFirst findings in pericardial disease, must go back to basicsRemember that superior portion of LA and pulmonary veins are extra-pericardial structures.
2/ In constrictive pericarditis (CP) or cardiac tamponade (CT), inspiratory
of intra-thoracic pressure & in PVeins is not transmitted to LA or LV. This dissociation leads toPVein-LA gradient and LV filling, demonstrated by an inspiratory in mitral inflow velocity by >25%.
of intra-thoracic pressure & in PVeins is not transmitted to LA or LV. This dissociation leads toPVein-LA gradient and LV filling, demonstrated by an inspiratory in mitral inflow velocity by >25%.
3/ In CP. early diastolic septal "bounce" is noted in 2D and M-mode. M-mode also reveals rapid relaxation of posterior wall followed by "flattening" of motion throughout diastole. Ventricular interdependence seen in CP and CT, septum shifts L in inspiration and R in expiration.
4/ In restriction, tissue Doppler is abnormal (e' and 
E/e') but in constriction e' is preserved and often higher in the septal annulus rather than lateral which can be tethered by the thickened pericardium ("annulus reversus" or "annulus paradoxus") as seen in our case.
e' and E/e') but in constriction e' is preserved and often higher in the septal annulus rather than lateral which can be tethered by the thickened pericardium ("annulus reversus" or "annulus paradoxus") as seen in our case.
5/ PWD of the hepatic veins (HV) reveals expiratory diastolic flow reversal in both CP and CT. This is due to LV interdependence and septum shifting to the R in expiration, not allowing RV to fully expand in diastole. Demonstrated here (respirometer tracing not great, sorry...).
6/ So how do we differentiate CP from CT? First thing is of course the presence of significant pericardial effusion, clinical picture (pulsus paradoxus vs Kussmaul's sign), and R chamber collapse (for RA >30% of cardiac cycle). This case has an effusion but no definite collapse.
7/ Mitral inflow & HV flow can help differentiate CT from pure CP and effusive-constrictive pericarditis (ECP). All with insp reversal:
CT: lower E/A ratio, 
HV diast forward flow
CP: E>A, prominent HV diast forward flow
ECP: Intermediate (+ organized/echogenic effusion?)
CT: lower E/A ratio, HV diast forward flowCP: E>A, prominent HV diast forward flowECP: Intermediate (+ organized/echogenic effusion?)
8/ So though CT, CP and ECP all display inspiratory decrease in mitral inflow and diastolic flow reversal in hepatic veins, PWD patterns in mitral inflow and HV are not the same!
See excellent paper by @JaeKOh2 et al on this subject: https://academic.oup.com/ehjcimaging/article/20/3/298/5049591
See excellent paper by @JaeKOh2 et al on this subject: https://academic.oup.com/ehjcimaging/article/20/3/298/5049591
9/ End of " #tweetorial. Subtle cases of constrictive pericarditis can often be missed if not paying attention to these details. And differentiation of cardiac tamponade and constrictive physiology in patients with pericardial effusion is not always easy! I hope this was helpful.
