Acute aortic regurgitation results in acute volume overload of a normal sized left ventricle (LV).1 Because of acute onset, LV remodeling has no time to develop, so the combined large aortic regurgitant flow and left atrial inflow result in abruptly increased left ventricular (LV) end-diastolic pressure.2 Left ventricle volume overload can result clinically in an “arterial hyperpulsatility,” also called “cardiac erethism.”3,4 We hypothesized that the arterial hyperpulsatility secondary to acute severe aortic regurgitation could be quantified using transesophageal echocardiography at the level of the aortic isthmus (initial portion of the descending thoracic aorta).