1. Hemodynamics of constrictive pericarditis

2. Restrictive physiology
Restrictive physiology is characterised by impediment to ventricular filling caused by
Increased ventricular stiffness-RCM
Increased pericardial restraint-CCP
Constrictive pericarditis and restrictive cardiomyopathy share clinical features and hemodynamic findings

3. Preserved systolic function.
Grade III diastolic dysfunction.
Elevation and equalization of diastolic pressures
Dip and plateau pattern in Ventricular pressure tracing

4. Pericardium

5. Pericardium-2 layers
Visceral-monolayer of mesothelial cells ,collagen &elastin fibres
Parietal layer-collagen and elastin fibres
Visceral layer reflects back over origins of great vessels
LA largely extrapericardial

6. Pericardium-physiology

7. Pericardium can restrain cardiac volume
Contact pressure exerted on the heart can limit filling when upper limit of normal cardiac volume exceeded
Contribute to diastolic interaction b/w cardiac chambers

9. Constrictive pericarditis
Scarring of both visceral and parietal layers constraining cardiac chambers
Causes
Tuberculosis
Ideopathic or viral pericarditis
Mediastinal irradiation
Open heart surgery
CRF
Connective tissue disorders

10. CCP-pathophysiology Marked restriction of filling
Ventricular interdependence
Failure of transmission of intrathoracic pressures to intracardiac chambers

11. Restriction to cardiac filling
Physiologic effect produced by constricting pericardium
Gradual devt of systemic and pulmonary venous hypertension
Atrial pressures mmHg-systemic venous congestion
18 to 30 mmHg-effort dyspnea,orthopnea
Fall in stroke volume
Increased HR,systemic vascular resistance
Inability to augment cardiac output during exercise-fatigue
Resting C.O.P falls-cachexia

12. Ventricular interdependence
Filling of one ventricle limits the simultaneous filling of other ventricle owing to the shared mechanical constraint
Coupled constraint-tamponade-greater ventricular interdependence
Uncoupled constraint-modest interdependence-predominant effect on the thin walled RV

13. Loss of transmission of intrathoracic pressures
Normal
Inspiratory decrease in ITP transmitted to all cardiac chambers
Decrease in pressure in pulmonary veins and LV
Decrease in PCWP accompanied by corresponding decrement in LV pressures
Gradient that drives LV filling maintained

14. Normal

15. CCP Pulmonary veins ,LA-extrapericardial
Inspiratory decrease in ITP transmitted to the pulmonary vein and LA but not to LV
Decrease in PCWP not accompanied by corresponding decrease in LV pressures
Less gradient that drives LV filling-inspiratory decrease in LV filling
Allows increased RV filling and IVS shift to left
Opposite occurs in expiration

16. . Hurrell D G et al. Circulation 1996;93:2007-2013
Copyright © American Heart Association

17. CCP

18. RA pressures

19. Restricted filling-elevation of mean pressure
Early diastole-rapid filling-prom. Y descent
Elevated RAP
Suction effect due to decreased ESV
Friedreich sign
Abrupt cessation of ventricular filling-nadir of Y descent
kussmaul s sign
Inspiratory increase in venous return-decr.ITP
Failure of transmission of decr.ITP to RV
Ventricular interdependence is modest

21. Ventricular pressure tracing

22. Equalisation of LV &RV pressures –ventricular interdependence
Early diastole
Filling of ventricles unimpeded
Rapid-high RAP,decreased ESV
Ventricular RFW >7 mmHg
Abrupt halt to ventricular filling once the limit set by the pericardium
Dip and plateau pattern
Equalisation of LV &RV pressures –ventricular interdependence

23. RVEDP>1/3 RVSP
Discordance b/w RVSP and LVSP during phases of respiration

27. FEATURE SENSITIVITY% SPECIFICITY%
LVEDP – RVEDP < 5mm Hg
RVEDP / RVSP > 1/
PA SP < 55 mm Hg
LV RFW > 7 mm Hg
RESPIRATORY ~ RAP < 3mm Hg
RESPIRATORY ~ PAWP – LV PG > 5mm Hg
LV – RV INTERDEPENDENCE
D G HURRELL CIRCULATION 1996

28. . Hurrell D G et al. Circulation 1996;93:2007-2013
Copyright © American Heart Association

30. Systolic area index
RV area/LV area in inspiration÷RV area /LV area in expiration
>1.1 s/o CCP

31. FEATURE SENSITIVITY% SPECIFICITY%
LVEDP – RVEDP < 5mm Hg
RVEDP / RVSP > 1/
PA SP < 55 mm Hg
LV RFW > 7 mm Hg
RESPIRATORY ~ RAP < 5mm Hg
SYSTOLIC AREA INDEX >
D R Talreja JACC 2008;51:315

32. Echo-M mode Septum- Postr wall Sharp EF slope in MV M-mode
Rapid movements in early diastole and atrial contraction
Postr wall
Abrupt postr motion in early diastole and flat in diastole
Sharp EF slope in MV M-mode

34. Echo Doppler Mitral peak E velocity>25 % increase in exp.
Tricuspid peak E velocity >25 % increase in insp.
DT<160 ms,IVRT<60 ms
E/A ratio >2

35. Echo features-doppler

37. PV doppler S <D Prominent atrial reversal
Incresed velocities in expiration

38. Mitral and PV flow in CCP(TEE)

39. Hepatic vein Doppler S<D in inspiration,S>D in expiration
Diastolic flow reversal in expiration

40. HV diastolic flow reversal in expiration

41. TDI
Mitral annular E’>8 cm/s
E/E’ <15

44. Variant forms Effusive constrictive Occult constriction
Failure of RAP to decline by at least 50% to a level below 10 mm Hg when pericardial pressure decreased to 0 by pericardiocentesis
Occult constriction
Features of constriction unmasked by volume expansion
Localised constriction
Transient constriction