It usually results from tuberculosis. Pyogenic, viral infection, Radiation, cardiac surgery and haemopericardium are less common causes. Rheumatic pericarditis may very rarely cause pericardial constriction.
PATHOLOGY AND HAEMODYNAMICS
The disease is the result of healing of tuberculous and any other fibrinous pericarditis. The fibrous tissue laid down with granulation tissue gradually forms a firm, constricting fibrous casing around the heart and very often it is calcified thus making the pericardial sac more rigid. As a result of interference with the cardiac filling, heart cannot dilate during diastole. The stroke output is almost fixed at a lower quantity so that increase in cardiac output is possible by increase in heart rate only. Renal retention of sodium and water also takes place.
Examination of the Heart
Precordium is quiet, Apex beat is invisible or very feeble. Sometimes there may be systolic indrawing or retraction of Apex of heart, As the ventricle is abruptly filled up there may be a diastolic shock. On auscultation triple rhythm is heard. The extra sound occurs in early diastole due to high pressure of ventricular filling and is called pericardial knock. S2 is widely split but respiratory variation is absent.
There may be ascites which may be out of proportion to pedal oedema. Liver is enlarged but not pulsatile. Chest may show evidences of pleural effusion.
INVESTIGATIONS | CHRONIC CONSTRICTIVE PERICARDITIS
DIFFERNTIAL DIAGNOSIS | CHRONIC CONSTRICTIVE PERICARDITIS
This is difficult. However left ventricular functions are depressed in cardiomyopathy and haemodynamically more complete equalization of diastolic pressure occurs in all four chambers in constrictive pericarditis.
Pericardial thickening and calcification in X-ray are also very valuable signs in favour of constrictive pericarditis.
In untreated cases it is always bad. Patient usually dies of low cardiac output or in some cases from hepatic insufficieney.
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