The initiation of bubble cavitation and subsequent stable bubble formation is thought to arise from low-pressure regions in vortices created by instantaneous valve closure and occluder rebound. We applied particle image velocimetry (PIV) in vitro to measure and reduce instantaneous plane flow fields into the vortex core radius, maximum tangential velocity, circulation strength, and pressure drop, to quantitatively analyze the role of vortices in cavitation. The Bjork-Shiley Monostrut 25 mm and the St. Jude Medical 25 mm were separately placed in the mitral position of a circulatory mock loop. Symmetric, vertical plane velocity fields in the center of each valve were measured via PIV. Time phases were set at 0.3, 2, 5, and 10 msec following impact of the occluder with the valve ring. The heart rate was set at 70, 90, and 120 bpm with respective cardiac outputs of 5, 6, and 7.5 L/min. The velocity profile of the vortex core identifies it as a Rankine vortex. The vortex strength rises at 0.3 to 2 msec, reflecting the rebound effect, and rapidly decreases at 10 msec, indicating viscous dissipation; vortex strength also intensifies with rising heart rate. Based on the Rankine vortex model, the maximum pressure drop at the center of the vortex is on the order of 40 mmHg. Cavitation and bubbles form when local flow field pressure drops below vapor pressure. Based on our results with a maximum pressure drop of merely 40 mmHg, this implies that the contribution of vortices in regurgitant flow is of little significance to cavitation formation.