BACKGROUND: To evaluate hemodynamic and functional changes of the failed left ventricle by Velocity Vector Imaging (VVI) and tissue Doppler, 22 patients with cardiogenic shock supported by extracorporeal life support (ECLS) were imaged during ECLS output variations inducing severe load manipulations. METHODS: The following data were acquired: (1) mean arterial pressure, aortic Doppler velocity-time integral, left ventricular end-diastolic volume, and mitral Doppler E wave; (2) tissue Doppler systolic (Sa) and early diastolic (Ea) velocities; and (3) systolic peak velocity (Sv), strain, and strain rate using VVI. RESULTS: Load variations were documented by a significant decrease in afterload (mean arterial pressure, -21%), an increase in preload (left ventricular end-diastolic volume, +12%; E, +46%; E/Ea ratio, +22%), and an increase in the velocity-time integral (+45%). VVI parameters increased (Sv, +36%; strain, +81%; and strain rate, +67%; P < .05), unlike tissue Doppler systolic velocities (+2%; P = NS). Whatever the ECLS flow, Sa was higher in patients who survived. CONCLUSIONS: VVI parameters are not useful in characterizing the failed left ventricle with rapidly varying load conditions. Tissue Doppler systolic velocities appear to be load independent and thus could help in the management of ECLS patients.
BACKGROUND: To evaluate hemodynamic and functional changes of the failed left ventricle by Velocity Vector Imaging (VVI) and tissue Doppler, 22 patients with cardiogenic shock supported by extracorporeal life support (ECLS) were imaged during ECLS output variations inducing severe load manipulations. METHODS: The following data were acquired: (1) mean arterial pressure, aortic Doppler velocity-time integral, left ventricular end-diastolic volume, and mitral Doppler E wave; (2) tissue Doppler systolic (Sa) and early diastolic (Ea) velocities; and (3) systolic peak velocity (Sv), strain, and strain rate using VVI. RESULTS: Load variations were documented by a significant decrease in afterload (mean arterial pressure, -21%), an increase in preload (left ventricular end-diastolic volume, +12%; E, +46%; E/Ea ratio, +22%), and an increase in the velocity-time integral (+45%). VVI parameters increased (Sv, +36%; strain, +81%; and strain rate, +67%; P < .05), unlike tissue Doppler systolic velocities (+2%; P = NS). Whatever the ECLS flow, Sa was higher in patients who survived. CONCLUSIONS: VVI parameters are not useful in characterizing the failed left ventricle with rapidly varying load conditions. Tissue Doppler systolic velocities appear to be load independent and thus could help in the management of ECLS patients.