The saturation of haemoglobin with oxygen is determined by the partial pressure of oxygen (P02) in the blood, the relationship between the two being described by the oxyhaemoglobin dissociation curve. The sigmoid shape of this curve is important clinically for a number of reasons:
• Falls in Pa02 may be tolerated provided that the percentage saturation remains above 90%.
• Increasing the Pa02 to above normal has only a minimal effect on oxygen content unless hyperbaric oxygen is administered (when the amount of oxygen in solution in plasma becomes significant).
• Once on the steep ‘slippery slope’ of the curve, a small decrease in Pa02 can cause large falls in oxygen content, while increasing Pa02 only slightly (e.g. by administering 28% oxygen to a patient with chronic bronchitis) can lead to useful increases in oxygen saturation.
The Pao2 is in turn influenced by the alveolar oxygen tension (PA02), the efficiency of pulmonary gas exchange, and the partial pressure of oxygen in mixed venous blood (PV<>2)·
Alveolar oxygen tension
The partial pressures of inspired gases. By the time the inspired gases reach the alveoli they are fully saturated with water vapour at body temperature (37°C), which has a partial pressure of 6.3 kPa (47 mmHg) and contains CO2 at a partial pressure of approximately 5.3 kPa (40 mmHg). The PA02 is thereby reduced to approximately l3.4 kPa (100 mmHg). The clinician can influence PA02 by administering oxygen or increasing the barometric pressure (i.e. administering hyperbaric oxygen). Because of the reciprocal relationship between the partial pressures of oxygen and carbon dioxide in the alveoli, a small increase in PA02 can be produced by lowering the PAC02 (e.g. using mechanical ventilation).
Pulmonary gas exchange
In normal subjects there is a small alveolar-arterial oxygen difference (PA-a02). This is due to:
• A small (0.133 kPa, 1 mmHg) pressure gradient across the alveolar membrane
• A small amount of blood (2% of total cardiac output) bypassing the lungs via the bronchial and thebesian veins
• A small ventilation/perfusion mismatch Pathologically there are three causes of a PA-a02 difference: DIFFUSION DEFECT. This is not an important cause of hypoxaemia even in conditions such as fibrosing alveolitis, in which the alveolar capillary membrane is considerably thickened. Certainly carbon dioxide is not affected, as it is much more soluble than oxygen.
RIGHT-TO-LEFT SHUNTS. In certain congenital cardiac lesions, e.g. Fallot’s tetralogy and when a segment of lung is completely unventilated, a large amount of blood bypasses the lungs and causes arterial hypoxaemia. This hypoxaemia cannot be corrected by administering oxygen to increase the PA02, because blood leaving normal alveoli is already fully saturated and further increases in P02 will not significantly affect its oxygen content. On the other hand, because of the shape of the carbon dioxide dissociation curve, the high Pco; of the shunted blood can be compensated for by overventilating patent alveoli, thus lowering the CO2 content of the effluent blood. Indeed, many patients with acute right-to-left shunts hyperventilate in response to the hypoxia or stimulation of mechanoreceptors in the lung, so that the Pac02 is normal or low.
VENTILATION/PERFUSION (VIQ) MISMATCH.This is discussed in more detail in Chapter 12. Diseases of the lung parenchyma result in a VIQ mismatch, producing an increase in alveolar dead space and hypoxaemia. The former can be compensated for by increasing overall ventilation. In contrast to the hypoxia resulting from a true right-to-Ieft shunt (see above), that due to areas of low VIQ can be partially corrected by administering oxygen and thereby increasing the PA02 even in poorly ventilated areas of lung.