Adequate organ function requires adequate provision of cells with oxygen (O2). The driving force for O2-diffusion from ambient air to its site of consumption in cell mitochondria is the oxygen partial pressure (pO2) gradient along this pathway. After uptake in the lungs, O2 transport in blood is achieved (1) through binding to haemoglobin and (2) through physical dissolution in plasma. While the sum of O2 in these two transport states defines total oxygen content of blood, the delivery of O2 to different organs is determined by cardiac output and arterial O2 content, being the product of both parameters. In the case of anaemia, intravascular volume and cardiac compensatory mechanisms determine the degree of O2 content reduction allowable prior tissue hypoxia and lactacidosis occur. When intravascular volume is preserved (e.g. normovolemic dilutional anaemia), reductions in O2 content are tolerated to a much higher degree than in hypovolemic anaemia (e.g. haemorrhagic shock).