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Hemodynamics of constrictive pericarditis. Restrictive physiology Restrictive physiology is characterised by impediment to ventricular filling caused.

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Presentation on theme: "Hemodynamics of constrictive pericarditis. Restrictive physiology Restrictive physiology is characterised by impediment to ventricular filling caused."— Presentation transcript:

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

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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 10-18 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

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21 Ventricular pressure tracing

22 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

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27 FEATURE SENSITIVITY% SPECIFICITY% LVEDP – RVEDP < 5mm Hg 60 38 RVEDP / RVSP > 1/3 93 38 PA SP < 55 mm Hg 93 24 LV RFW > 7 mm Hg 93 57 RESPIRATORY ~ RAP < 3mm Hg 93 48 RESPIRATORY ~ PAWP – LV PG > 5mm Hg 93 81 LV – RV INTERDEPENDENCE 100 95 D G HURRELL CIRCULATION 1996

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

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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 46 54 RVEDP / RVSP > 1/3 93 46 PA SP < 55 mm Hg 90 29 LV RFW > 7 mm Hg 45 44 RESPIRATORY ~ RAP < 5mm Hg 71 37 SYSTOLIC AREA INDEX >1.1 97 100 D R Talreja JACC 2008;51:315

32 Echo-M mode Septum- – 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

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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

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37 PV doppler S { "@context": "http://schema.org", "@type": "ImageObject", "contentUrl": "http://images.slideplayer.com/4200551/14/slides/slide_36.jpg", "name": "PV doppler S

38 Mitral and PV flow in CCP(TEE)

39 Hepatic vein Doppler 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

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44 Variant forms Effusive constrictive – 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


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