Left ventricular function in acute non-ischaemic mitral regurgitation.

摘要: Acute nonischaemic mitral regurgitation (MR) has recently generated considerable interest because of its causal relationship to ruptured chordae tendineae and infective endocarditis, advances in diagnosis by echo Doppler studies, management afterload reduction reconstructive surgery. It is fundamentally different from chronic MR the previously normal, unprepared left ventricle (LV) lefi atrium (LA) confront a sudden dramatic increase volume. As normal-sized suddently receives marked regurgitant flow, pressure rises transmitted into pulmonary capillaries causing congestion oedema. At onset, LV function usually well preserved oederna does not reflect failure. In acute MR, empties atrium, thus reducing radius systolic pressure, resulting decline wall tension according Laplace's law. With tension, there increme contractile shortening with total output. The may fail early severe it forced clilate rapidly before hypertrophy can occur, whereas both diastolic volume mass proportionately. persistence dysfunction failure occur as manifestation ‘cardiomyopathy overload’[1]. Fortunately low energy cost per unit work shortening, m opposed that used for development, only slight myocardial oxygen consumption MR. patients secondary ejection fraction be slightly decremed. end-systolic dimension more useful predictor than fraction. vasodilators intra-aortic balloon pump extremely effective impedance ejection, orifice