The patient with severe acute MR, which might occur from chordal rupture, usually experiences acute hemody- namic decompensation. The sudden volume overload increases LA and pulmonary venous pressures, leading to pulmonary congestion and hypoxia, whereas de- creased blood delivery to the tissues with a concomitant decrease in LV systolic pressure limits the pressure gradi- ent, driving MR to early systole. Thus, the murmur may be short and unimpressive, as may be the color jet of MR by TTE. In the presence of sudden acute and he- modynamic instability after myocardial infarction, with hyperdynamic LV function by TTE and no other cause for the deterioration, TEE can be especially helpful in detecting papillary muscle or chordal rupture or valvular vegetations and annular abscesses that may further ac- centuate the need for a more urgent surgical approach.1 7.1.2. Medical Therapy Vasodilator therapy improves hemodynamic compen- sation in acute MR. The premise for use of vasodila- tors in acute MR is a reduction in impedance of aortic flow, thereby preferentially guiding flow away from the LV-to-LA pathway, decreasing MR while simultaneously increasing forward output to the LV-to-aortic path- This is usually accomplished by infusion of an easily titratable agent, such as sodium nitroprusside or nicardipine. Use of vasodilators is often limited by sys- temic hypotension that is exacerbated when peripheral resistance is decreased. Intra-aortic balloon counterpul- sation can be helpful to treat acute severe MR. By low- ering systolic aortic pressure, intra-aortic balloon coun- terpulsation decreases LV afterload, increasing forward output while decreasing regurgitant volume. Simulta- neously, intra-aortic balloon counterpulsation increases diastolic and mean aortic pressures, thereby supporting the systemic circulation. The use of a percutaneous cir- culatory assist device may stabilize a patient with acute hemodynamic compromise before the procedure. 