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Constrictive pericarditis pathophysiology
This document discusses the pathophysiology of constrictive pericarditis (CCP). CCP is caused by a thickened and fibrotic pericardium that restricts heart filling. This leads to 4 key hemodynamic changes: 1) impaired diastolic filling, 2) dissociation of intrathoracic and intracardiac pressures with respiration, 3) excessive ventricular coupling, and 4) heart rate dependent filling. The thick pericardium equalizes pressures in all chambers and abruptly halts early diastolic filling. Inspiration decreases left ventricular filling while increasing right ventricular filling via septal shift. Expiration causes the opposite effect.
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Constrictive pericarditis pathophysiology
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- 4. ETIOLOGY OF CCP •Idiopathic • Infective – Tubercular • Bacterial : staphylococcal , strep, E coli, salmonella, H influenza, gonococcus, pneumococcal • Viral : adeno, coxsackie, influenza, lassa • Fungal:Histoplasma,coccidiomycosis,nocardia,aspergillosis,Blastomy cosis. • Others: Guinea worm infestation, hydatid disease , amebiasis, whipple disease • Trauma: Blunt: steering wheel injury, CPR • Penetrating injury: stabs, bullets • Impalement injury, cardiopericardial surgery • Intrapericardial electrodes,pacing electrodes and AICD devices
- 5. Autoimmune: SLE, rheumatoidarthritis, polyserositis, scleroderma Irradiation Neoplastic: Mesothelioma, undifferentiated carcinoma, melanoma, metastasis. Drugs: Methysergide, procainamide, mitomycin C, Hydralasine Dialysis related, congenital : mulibreynanism, afibrinogenemia Asbestosis, amyloidosis, Sarcoidosis, campylobacter, whipples disease. Post infarction, post hemopericardium, dresslars.
- 6. Peel described fourstages in the development of constriction Dry stage Stage of effusion Stage of absorption Stage of pericardial constriction
- 7. Summarizing Features ofvariant forms of constrictive pericarditis Effusive- constrictive pericarditis Pericardial effusion is present, sometimes loculated, with constriction by the visceral pericardium Occult constrictive pericarditis Haemodynamics are normal at rest, but assume the features of constriction after an acute volume load Localised constrictive pericarditis Constriction limited to the right or left ventricle. Ventricular interdependence reduced or absent Transient constrictive pericarditis During the resolution of acute pericarditis with effusion, constriction develops, but then resolves spontaneously over a few weeks
- 8. Basic pathology inCCP is the inability of the ventricles to dilate due to the thick fibrous envelope around the heart
- 9. Four hemodynamic changesin CCP • Impaired diastolic filling • Dissociation of intrathoracic and intracardiac pressures • Excessive ventricular coupling • Heart rate dependent filling
- 10. Fibrosed thickened calcifiedpericardium restricts the diastolic filling of all the chambers and determines the diastolic volume of the heart Symmetrical constricting effect results in elevation and equalization of diastolic pressures in all four chambers. Early diastolic filling is unimpeded and hence there is early rapid filling It is abruptly halted when the intra cardiac volume reaches the limit set by a noncompliant pericardium
- 11. Avasthe ,Wasir, MLBhatia, Sujoy B Roy AIIMS,JIMA 1968 Concluded that haemodynamic effects of CP is due to mechanical limitation of ventricular filling and possibly also to emptying of the ventricle if the myocardium is involved The ventricular function is depressed due to -Myocardial atrophy -Myocardial fibrosis -Obliteration of coronary arteries in the fibrotic pericardium causing myocardial ischemia -Coexistent CMP
- 12. Grover,Bhatia ,Sujoy ,AIIMSIHJ 1972 Described presence of myocardial factor --- incriminated it as a cause for incomplete symptomatic improvement following surgery Sukumar et al 1966 reported that a delayed early dip and a slow rising EDP in the ventricular tracing of a patient with CCP suggests co existing myocardial disease.
- 13. Impaired diastolic filling-sqaure root
- 14. Dissociation of intrathoracicand intracardiac pressures with respiration In a normal person , the Pressure in the intrathoracic cavity at peak inspiration –6 at peak expiration –3 This decrease in the intrathoracic pressure is normally transmitted to all the cardiac chambers and the pulmonary veins . Thus in normal subjects pressure gradient between PVs and LA is relatively unchanged, there is no change in the driving pressures from the lung to the left sided chambers , there fore the flow is maintained in both inspiration and expiration.
- 15. What happens InCCP Because of the encasing rigid pericardium , the intrathoracic pressures changes are not transmitted to the left cardiac chambers Hence the gradient between PVs and LA decreases(in inspiration ), there is low driving force from the lung in to LA, therefore Inspiratory redution in the velocity of diastolic flow in the PVs Reduction in the left sided filling in inspiration Reduced transmitral gradient : reduced velocity across mitral valve Inspiratory increase in peak tricuspid flow velocity Opposite changes occur during expiration , that is more driving force causing more LV filling
- 16. 2.Ventricular interaction (ventricular coupling) Ventricles of the heart share a common septal wall, are encircled by common fibres ,and are enclosed within the pericardial cavity Because of the close anatomical relationship ,the volume or pressure in one ventricle can directly influence the volume and pressure in the other ventricle
- 17. Henderson and Prince IncreasingRV volume shifted the IVS towards the LV and altered the LV filling characterstics . The coupling is greatly increased in the prescense of intact pericardium
- 18. What happens InCCP Total amount of blood entering the heart is nearly constant Therefore inspiratory reduction in LV filling is associated with a simultaneous increase in RV diastolic filling , and the septum moves leftward . Opposite effects occur in expiration
- 19. Expiration ( increasein intrathoracic pressure ) Cardiac chambers remain isolated of the pressure changes But PVs and venacavae are influenced Flow in LV increases Septum shifts to the right
- 20. -On Expiration- -There isreduction in flow velocity in the venacavae -Increased hepatic venous diastolic flow reversal -Decreased transtricuspid flow velocity
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- 23. Which is paradox? Kussmaul? Pulsus paradoxus ?
- 54. A DECISION IS ASIMPORTANT AS AN INCISION Thank you