Constrictive pericarditis

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With regarding to pathophysiology of constrictive pericarditis put the following in order:

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Venous return to the heart becomes limited, and ventricular filling is reduced, with associated inability to maintain adequate preload.

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

Because of these changes, the potential space between the linings is obliterated, and the ventricle loses distensibility.

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

In constrictive pericarditis, the easily distensible, thin parietal and visceral pericardial linings become inflamed, thickened, and fused.


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