The cardiovascular response in sepsis is the result of subcellular dysfunction and impaired metabolism from the complex interaction of cytokine and mediator with cellular involvement. The typical cardiovascular abnormalities seen are tachycardia, hypotension (relative decrease in preload), increased cardiac index, decrease in left ventricular stroke work index, decrease in ejection fraction (which is load dependent), and an apparent decrease in contractility. After augmentation of preload, the ventricles dilate in a response similar to the Frank-Starling mechanism. By challenging these patients with the augmentation of preload and contractility to increase oxygen delivery would theoretically minimize microcirculatory dysfunction and lactic acid production. Survivors have an amplification of this biventricular response. This response would temporarily normalize within a week, while the nonsurvivors would still have increased hemodynamics (tachycardia) without the ventricular dilation as a compensatory response. Even though the survivor response is not predictable, therapeutic end-points have been proposed as a guide to therapy in these critically ill patients. Conflicting results have been reported regarding contractility and ventricular compliance measurements in septic models. The development of pressure-volume loops would be the ideal technique for the evaluation of ventricular diastolic compliance, true preload, and contractility (from the end-systolic pressure relationship, which is load independent) in sepsis. More research has to be done with this type of evaluation to further understand the dynamic cardiovascular response in sepsis. This question still persists. Why can't some patients be hemodynamically challenged to increase right and left ventricular end-diastolic volumes and oxygen delivery?