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Hemodynamics of Constrictive Pericarditis - DR Deepak Raju

The document discusses the hemodynamics of constrictive pericarditis. It restricts cardiac filling and causes elevation of pressures. Key findings include elevated and equalized diastolic pressures, a dip and plateau in ventricular pressures, and loss of transmission of intrathoracic pressures between the ventricles.

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Muhammad Jazib
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24 views44 pages

Hemodynamics of Constrictive Pericarditis - DR Deepak Raju

The document discusses the hemodynamics of constrictive pericarditis. It restricts cardiac filling and causes elevation of pressures. Key findings include elevated and equalized diastolic pressures, a dip and plateau in ventricular pressures, and loss of transmission of intrathoracic pressures between the ventricles.

Uploaded by

Muhammad Jazib
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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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
• 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-
– 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
– 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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