Alveolar Po₂ is determined by dry barometric pressure, inspired oxygen concentration and the ratio of oxygen consumption to alveolar ventilation (page 139). Assuming that the first two are unchanged, and there being good evidence that the latter two factors are unaffected in the resting state by anaemia down to a haemoglobin concentration of at least 5 g.dl⁻¹ (see below), then there is no reason why alveolar Po₂ or Pco₂ should be affected by uncomplicated anaemia down to this degree of severity.

The increased cardiac output (see below) will cause a small reduction in pulmonary capillary transit time which, together with the reduced mass of haemoglobin in the pulmonary capillaries, causes a modest decrease in diffusing capacity (page 152). However, such is the reserve in the capacity of pulmonary capillary blood to reach equilibrium with the alveolar gas (see Figure 9.2) that it is highly unlikely that this would have any measurable effect on the alveolar/end-pulmonary capillary Po₂ gradient, which in the normal subject is believed to be of the order of only 10⁻⁶ mmHg. Thus pulmonary end-capillary Po₂ should also be normal in anaemia.

Continuing down the cascade of oxygen partial pressures from ambient air to the site of use in the tissues, the next step is the gradient in Po₂ between pulmonary end-capillary blood and mixed arterial blood. The Po₂ gradient at this stage is caused by shunting and the perfusion of relatively underventilated alveoli. There is no evidence that these factors are altered in anaemia, and arterial Po₂ should therefore be normal. Because the peripheral chemoreceptors are stimulated by reduction in arterial Po₂ and not arterial oxygen content (page 71), then there should be no stimulation of respiration unless the degree of hypoxia is sufficient to cause anaerobic metabolism and lactacidosis.

It is well established that red blood cell 2,3-diphosphoglycerate levels are increased in anaemia (page 194), typical changes being from a normal value of 5 mmol.l⁻¹ to 7 mmol.l⁻¹ at a haemoglobin concentration of 6 g.dl⁻¹.¹ This results in an increase in P₅₀ from 3.6 to 4.0 kPa (27 to 30 mmHg). This rightward shift of the dissociation curve would have a negligible effect on arterial saturation, which has indeed been reported to be normal in anaemia. The rightward shift will, however, increase the Po₂ at which oxygen is unloaded in the tissues, mitigating to a small extent the effects of reduction in oxygen delivery so far as tissue Po₂ is concerned.

Although the arterial oxygen saturation usually remains normal in anaemia, the oxygen content of the arterial blood will be reduced in approximate proportion to the decrease in haemoglobin concentration. Arterial oxygen content can be expressed as follows:

(1)

where Cao₂ is arterial oxygen content, [Hb] is haemoglobin concentration, Sao₂ is arterial oxygen saturation, 1.39 is the combining power of haemoglobin with oxygen (page 189) and 0.3 is dissolved oxygen at normal arterial Po₂.

Equation (3) shows that, if other factors remain the same, a reduction in haemoglobin concentration will result in a proportionate reduction in oxygen delivery. Thus a haemoglobin concentration of 7.5 g.dl⁻¹, with unchanged cardiac output, would halve delivery to give a resting value of 500 ml.min⁻¹

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