Hemodynamics of constrictive pericarditis

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

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

Pericardium

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

Pericardium-physiology

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

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

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

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

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

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

Normal

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

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

CCP

RA pressures

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

Ventricular pressure tracing

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

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

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

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

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

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

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

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

Echo features-doppler

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

Mitral and PV flow in CCP(TEE)

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

HV diastolic flow reversal in expiration

TDI Mitral annular E’>8 cm/s E/E’ <15

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