There is increasing interest in the use of respiratory variations in vascular pressures (CVP, arterial and wedge pressure) to predict the cardiac output response to a fluid challenge. In patients receiving mechanical ventilation with no spontaneous efforts, continuous monitoring consistently demonstrates an early inspiratory rise in arterial pressure5(“reversed pulsus paradoxus”6), which is followed during late inspiration and expiration by a decrease in systolic pressure. Perel and Segal5 defined the difference between maximum and minimum arterial systolic pressure during a respiratory cycle as systolic pressure variation. The inspiratory increase in pressure relative to the value at end-expiration was called dUp, and the fall in pressure relative to the end-expiratory value was called dDown. While dUp reflects a direct mechanical effect of positive pressure on the ventricle, dDown is an index of preload reserve. The larger the dDown and pressure variation, the greater the predicted increase in cardiac output with volume loading. Based on similar considerations on the interplay between respiration and stroke volume, other variables such as stroke volume variation (SVV),,4 which can be measured by the commercially available PiCCO system (PiCCO plus; Pulsion Medical Systems; Munich, Germany), or aortic blood velocity variation (ABVV),3 have been shown to predict the hemodynamic effects of volume expansion on cardiac output as well. Basically, all of these new techniques (pulse pressure variation [PPV], SVV, ABVV) are predicated on the observation that the magnitude of the cyclic variation in stroke volume depends on whether the patient is operating on the steep or the flat portion of the Frank-Starling curve; that is, whether the heart is preload responsive or not.