Global oxygen delivery (D o 2) is the total amount of oxygen delivered to the tissues per minute irrespective of the distribution of blood flow. Under resting conditions with normal distribution of cardiac output it is more than adequate to meet the total oxygen requirements of the tissues (V o 2) and ensure that aerobic metabolism is maintained.
Recognition of inadequate global D o 2 can be difficult in the early stages because the clinical features are often non-specific. Progressive metabolic acidosis, hyperlactataemia, and falling mixed venous oxygen saturation (Sv o 2), as well as organ specific features such as oliguria and impaired level of consciousness, suggest inadequate D o 2. Serial lactate measurements can indicate both progression of the underlying problem and the response to treatment. Raised lactate levels (>2 mmol/l) may be caused by either increased production or reduced hepatic metabolism. Both mechanisms frequently apply in the critically ill patient since a marked reduction in D o 2 produces global tissue ischaemia and impairs liver function.
Table 1 ? illustrates the calculation of D o 2 from the oxygen content of arterial blood (Ca o 2) and cardiac output (Qt) with examples for a normal subject and a patient presenting with hypoxaemia, anaemia, and a reduced Qt. The effects of providing an increased inspired oxygen concentration, red blood cell transfusion, and increasing cardiac output are shown. This emphasises that: (1) D o 2 may be compromised by anaemia, oxygen desaturation, and a low cardiac output, either singly or in combination; (2) global D o 2 depends on oxygen saturation rather than partial pressure and there is therefore little extra benefit in increasing Pa o 2 above 9 kPa since, due to the sigmoid shape of the oxyhaemoglobin dissociation curve, over 90% of haemoglobin (Hb) is already saturated with oxygen at that level. This does not apply to the diffusive component of oxygen transport that does depend on the gradient of oxygen partial pressure.
Relative effects of changes in Pa o 2, haemoglobin (Hb), and cardiac output (Qt) on oxygen delivery (D o 2)
Although blood transfusion to polycythaemic levels might seem an appropriate way to increase D o 2, blood viscosity increases markedly above 100 g/l. This impairs flow and oxygen delivery, particularly in smaller vessels and when the perfusion pressure is reduced, and will therefore exacerbate tissue hypoxia. 1 Recent evidence suggests that even the traditionally accepted Hb concentration for critically ill patients of approximately 100 g/l may be too high since an improved outcome was observed if Hb was maintained between 70 and 90 g/l with the exception of patients with coronary artery disease in whom a level of 100 g/l remains appropriate. 2 With the appropriate Hb achieved by transfusion, and since the oxygen saturation (Sa o 2) can usually be maintained above 90% with supplemental oxygen (or if necessary by intubation and mechanical ventilation), cardiac output is the variable that is most often manipulated to achieve the desired global D o 2 levels.
Global oxygen consumption (V o 2) measures the total amount of oxygen consumed by the tissues per minute. It can be measured directly from inspired and mixed expired oxygen concentrations and expired minute volume, or derived from the cardiac output (Qt) and arterial and venous oxygen contents:
Directly measured V o 2 is slightly greater than the derived value that does not include alveolar oxygen consumption. 2 and D o 2 to avoid problems of mathematical linkage. 3