Oxygen therapy.

DO2 = CaO2 × cardiac output where CaO2 is total oxygen content, made up largely of oxygen bound to haemoglobin and, to a much smaller degree, oxygen dissolved in plasma. DO2 therefore depends not only on the degree of oxygenation of the blood but also on cardiovascular function and haemoglobin concentration. Despite its importance, it is not the most tightly regulated physiological parameter for metabolism and gas exchange. This is well illustrated by a study of repeated venesection resulting in isovolaemic anaemia (5 g/dl) in healthy humans.1 While cardiac output rose, it was insufficient to maintain DO2 but because of the steep slope of the oxyhaemoglobin dissociation curve at the tissue level, the fall in DO2 was offset by increased oxygen extraction, indicated by a reduction in mixed venous oxygen (SvO2). SvO2 is therefore a much better indicator of oxygen delivery than arterial saturation (SaO2), and is one of the targets in resuscitation in sepsis. SaO2 is readily measurable and helpful in resuscitation, although attention should be paid to integrated physiological function.2 The normal ranges of arterial oxygen tension (PaO2) and SaO2 are 10–13 kPa and 94–98%, respectively. It is apparent that DO2 cannot be significantly enhanced by increasing PaO2 above 16 kPa, where haemoglobin is 100% saturated and the amount of oxygen dissolved in the plasma is small. This manoeuvre will maximise CaO2 but may not always optimise DO2.