Shock comprises of circulatory insufficiency accompanied by a discrepancy between oxygen demand and supply at tissue level. This results in tissue hypoxia, which when persisting, can lead to (severe) organ failure. In this article we will discuss pathophysiologic backgrounds of shock following the mechanisms that cause hemodynamic deterioration and tissue hypoxia. Subsequently the role of various cytokines in the pathogenesis of septic shock, which occurs relatively frequent in childhood, are discussed. As far as fluid substitution and vasoactive medication is concerned, therapeutic strategies can be chosen more rationally these days. This is mainly due to the availability of smaller i.v. cannula, central venous catheters and advances in (non) invasive hemodynamic measurements in childhood e.g. central venous pressure, cardiac output, peripheral vascular resistance and left ventricular shortening fraction. Despite these developments, shock (in particular septic shock) remains to have a high mortality, also in childhood.