Abstract
Adequate organ function requires adequate provision of cells with oxygen (O 2). The driving force for O 2-diffusion from ambient air to its site of consumption in cell mitochondria is the oxygen partial pressure (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 these two transport states defines total oxygen content of blood, the delivery of O 2 to different organs is determined by cardiac output and arterial O 2 content, being the product of both parameters. In the case 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. haemorrhagic shock).
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