1Hemodynamics of constrictive pericarditis dr deepak raju

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 intrathoracicpressures 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 intrathoracicpressures

• 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-inspiratorydecrease in LV filling

– Allows increased RV filling and IVS shift to left

– Opposite occurs in expiration

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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

• 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

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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-

– Rapid movements in early diastole and atrialcontraction

• 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– 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