Septic shock, similar to other types of circulatory shock, is characterised by peripheral hypoperfusion and, consequently, inadequate tissue oxygen deli very. It is commonly believed that intravenous fluid infusion improves organ perfusion and reverses cel lular dysoxia. This belief might be valid in the early phase of septic shock, and some earlier studies [1] and international recommendations (Surviving Sepsis Campaign) [2] support this view. The physio logical rationale behind fluid bolus administration is that it causes intravascular volume expansion. According to the FrankStarling principle, increased left ventricular enddiastolic volume (i.e., preload) increases stroke volume (SV), resulting in improved organ perfusion. This mechanism works until the optimal preload is achieved. However, the patho physiology of septic shock is complex and compris es both distributive and cardiogenic components. At the peripheral level, the inflammatory process in sepsis damages the endothelial glycocalyx [3] and