Adequate organ function requires adequate provision of cells with oxyg
en (O-2). The driving force for O-2-diffusion from ambient air to its
site of consumption in cell mitochondria is the oxygen partial pressur
e (pO(2)) gradient along this pathway. After uptake in the lungs, O-2
transport in blood is achieved (1) through binding to haemoglobin and
(2) through physical dissolution in plasma. While the sum of O-2 in th
ese two transport states defines total oxygen content of blood, the de
livery of O-2 to different organs is determined by cardiac output and
arterial O-2 content, being the product of both parameters. In the cas
e of anaemia, intravascular volume and cardiac compensatory mechanisms
determine the degree of O-2 content reduction allowable prior tissue
hypoxia and lactacidosis occur. When intravascular volume is preserved
(e.g. normovolemic dilutional anaemia), reductions in O-2 content are
tolerated to a much higher degree than in hypovolemic anaemia (e.g. h
aemorrhagic shock). (C) 1997 Elsevier Science Ltd.