Acute and subacute forms of pericarditis (which may or may not be symptomatic) may deposit fibrin, which, in turn, can evoke a pericardial effusion.
This often leads to pericardial organization, chronic fibrotic scarring, and calcification, most often involving the parietal pericardium
In constrictive pericarditis, the easily distensible, thin parietal and visceral pericardial linings become inflamed, thickened, and fused.
Because of these changes, the potential space between the linings is obliterated, and the ventricle loses distensibility.
Venous return to the heart becomes limited, and ventricular filling is reduced, with associated inability to maintain adequate preload.
Filling pressures of the heart tend to become equal in both the ventricles and the atria.
Since the myocardium is unaffected, early ventricular filling during the first third of diastole is unimpeded
Elevated jugular venous pressures are an almost universal finding Sinus tachycardia is common while the blood pressure is normal or low, depending on the stage of the disease process
The apical impulse is often impalpable, and the patient may have distant or muffled heart sounds. A friction rub is usually not found
A pericardial knock, which corresponds with the sudden cessation of ventricular filling early in diastole, occurs in approximately half the cases. o It is usually heard along the left sternal border and may be mistaken for an S3 gallop
The Kussmaul sign (ie, elevation of systemic venous pressures with inspiration) is a common nonspecific finding,
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