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CONSTRICTIVE PERICARDITIS

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Slide 1 :

CONSTRICTIVE PERICARDITIS And other diseases of the pericardial sac

Slide 2 :

The normal pericardium is a fibroelastic sac containing a thin layer of fluid that surrounds the heart. When larger amounts of fluid accumulate (pericardial effusion) or when the pericardium becomes scarred and inelastic, one of three pericardial compressive syndromes may occur

Slide 3 :

Cardiac tamponade — Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure Constrictive pericarditis — Constrictive pericarditis is the result of scarring and consequent loss of elasticity of the pericardial sac Effusive-constrictive pericarditis — This variant is characterized by constrictive physiology with a coexisting pericardial effusion, usually with tamponade

Slide 4 :

MAIN POINT In the pericardial compressive syndromes, the pericardium is inelastic and total cardiac volume cannot change The result is enhanced ventricular interaction or… ventricular interdependence

Slide 5 :

normally 100 100

Slide 6 :

In constriction How much blood is in the RV??? 140

Slide 7 :

Again… How much blood is in the RV now??? 70

Slide 8 :

Belaboring the point.. Answer is? 85

Slide 9 :

Last time 150 Anyone?

Slide 10 :

Hemodynamics - Constriction In normal hemodynamics, inspiration causes a drop in intrathoracic pressure which is transmitted to the lungs AND heart Thus, pressure gradients from pulmonary veins to left ventricle are unchanged by inspiration In constrictive pericarditis, this drop in pressure is transmitted to the lungs BUT NOT THE HEART So, the pressure in the pulmonary veins drops while the pressure in the heart does not Thus, less blood fills the left ventricle

Slide 11 :

Hemodynamics - Constriction And because of ventricular interdependence, the right ventricular volume is increased OF NOTE: This is the reason that the RV filling is increased. It is NOT due to increased venous return because the inspiratory drop in pressure is NOT transmitted to the right atrium.

Slide 12 :

Hemodynamics - Tamponade In tamponade, inspiratory pressures ARE transmitted to the lungs and heart Thus, the mechanism of decreased LV stroke volume for constriction does not apply In tamponade, inspiration DOES increase venous return to the right heart So, because of ventricular interdependence. . . . . . .

Slide 13 :

Hemodynamics - Conclusion The net effect in both syndromes is a decreased LV stroke volume during inspiration and subsequent drop in pressure (which is measured as a pulsus paradoxus) The effect is much stronger in tamponade and thus pulsus paradoxus much more common in tamponade than constriction

Slide 14 :

That’s all I really wanted to say But here’s more if you want it

Slide 15 :

Constricitve Pericarditis - Etiology Idiopathic or viral — 42 to 49 percent Following cardiac surgery — 11 to 37 percent Following radiation therapy — 9 to 31 percent Connective tissue disorder — 3 to 7 percent Postinfectious (tuberculous or purulent pericarditis) — 3 to 6 percent Miscellaneous causes (malignancy, trauma, drug-induced, asbestosis, sarcoidosis, uremic pericarditis) — 1 to 10 percent

Slide 16 :

Constrictive Pericarditis - HPI 67 percent presented with symptoms of heart failure (HF) 8 percent with chest pain 6 percent with abdominal symptoms 4 percent with atrial arrhythmia 5 percent with symptoms of cardiac tamponade

Slide 17 :

Constricitve Pericarditis - PE Elevated JVP A, V, X, Y peaks and descents exist peripheral edema Ascites pulsatile hepatomegaly pleural effusion S3 Pulsus paradoxus is not that common Kussmaul’s sign is not sens/spec Cachexia may occur in late stages

Slide 18 :

Constrictive Pericarditis - ECHO Abrupt posterior motion of the ventricular septum in early diastole with inspiration (septal shudder and bounce) is caused by underfilling of the left ventricle (due to the decreased pulmonary vein-left atrial gradient with inspiration), allowing redistribution of blood from the left to the right ventricle M-mode may show notching of the ventricular septum in early diastole or with atrial systole due to transient reversal of ventricular septal transmural pressure at these times in the cardiac cycle

Slide 19 :

Constrictive Pericarditis - ECHO Other M-mode signs include rapid posterior motion of the left ventricular posterior wall in early diastole followed by a flattening (also a feature of restrictive cardiomyopathy), rapid left atrial emptying, and premature opening of the pulmonic valve (as right ventricular diastolic pressure rises above pulmonary arterial pressure). Two-dimensional echocardiography reveals dilation and absent or diminished collapse of the inferior vena cava and hepatic veins (plethora), moderate biatrial enlargement, a sharp halt in ventricular diastolic filling, hypermobile atrioventricular valves, and an abnormal contour between the posterior left ventricular the left atrial posterior walls

Slide 20 :

Constrictive Pericarditis - ECHO High E velocity of right and left ventricular (LV) inflow, due to the abnormally rapid early diastolic filling associated with the combination of a small volume and rapidly recoiling ventricle Tissue Doppler shows a prominent E (unless slowed by mitral annular calcification), which is an important point of distinction from restrictive cardiomyopathy in which the transmitral E is tall and narrow but the tissue E is diminutive

Slide 21 :

Constrictive Pericarditis - ECHO The usually positive linear relation between E/tissue E and left atrial pressure, which is useful for assessing left atrial pressure in cardiomyopathy is reversed (annular paradox) in constrictive pericarditis The propagation velocity of early diastolic transmitral flow on color M-mode is normal or increased

Slide 22 :

Constrictive Pericarditis - ECHO Mitral inflow velocity falls as much as 25 to 40 percent and tricuspid velocity greatly increases in the first beat after inspiration. The respiratory variation in pulmonary venous flow is even more pronounced Hepatic vein flow reversal increases with expiration, reflecting the ventricular interaction and the dissociation of intracardiac and intrathoracic pressures

Slide 23 :

Constrictive Pericarditis - ECHO The bottom line is that no sign or combination of signs is diagnostic of constrictive pericarditis However, a normal study virtually rules out the diagnosis

Slide 24 :

Constrictive Pericarditis – Tests? CT – not very sens/spec Cardiac MRI – growing in favor BNP – usually only a mild elevation due to limited wall stretch Cath – GOLD STANDARD

Slide 25 :

Constrictive Pericarditis - CATH Increased right atrial pressure Prominent x and y descents of venous and atrial pressure tracings Increased RV end-diastolic pressure, usually to a level one-third or more of RV systolic pressure "Square root" signs in the RV and LV diastolic pressure tracings A greater inspiratory fall in pulmonary capillary wedge pressure compared to left ventricular diastolic pressure Equalization of LV and RV diastolic plateau pressure tracings Discordance between RV and peak LV systolic pressures during inspiration

Slide 26 :

Cath tracings

Slide 27 :

Cath tracings

Slide 28 :

ventricular interdependence THE END

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Y peaks and descents exist; peripheral edema; Ascites; pulsatile hepatomegaly; pleural effusion ; S more Y peaks and descents exist; peripheral edema; Ascites; pulsatile hepatomegaly; pleural effusion ; S3; Pulsus paradoxus is not that common; Kussmaul’s sign is not sens/spec; Cachexia may less