Enlarged pulsatile liver is seen in-

Most commonly, TR is secondary to marked dilation of the tricuspid annulus from RV enlargement due to PA hypeension. Functional TR may complicate RV enlargement of any cause, including an inferior MI that involves the RV. It is commonly seen in the late stages of hea failure due to rheumatic or congenital hea disease with severe PA hypeension (pulmonary aery systolic pressure >55 mmHg), as well as in ischemic and idiopathic dilated cardiomyopathies. It is reversible in pa if PA hypeension can be relieved. Rheumatic fever may produce organic (primary) TR, often associated with TS. Infarction of RV papillary muscles, tricuspid valve prolapse, carcinoid hea disease, endomyocardial fibrosis, radiation, infective endocarditis, and trauma all may produce TR. As is the case for TS, the clinical features of TR result primarily from systemic venous congestion and reduction of CO. With the onset of TR in patients with PA hypeension, symptoms of pulmonary congestion diminish, but the clinical manifestations of right-sided hea failure become intensified. The neck veins are distended with prominent v waves and rapid y descents, marked hepatomegaly, ascites, pleural effusions, edema, systolic pulsations of the liver, and a positive hepatojugular reflex. ref : Harrison&;s principle of internal medicine,20 th edition,pg no.1948