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Measurement of the Gas-Exchanging Function of the Lung

In recent years methods for obtaining arterial blood by single puncture or by catheterization (Berneus et al. 1954) have become common. Gaseous equilibration methods (Denison et al. 1969) have allowed access to the mixed venous gas pressures. More detailed values for the normal arterial 02 and CO2 pressures have also been published (Mellemgaard 1966). Recent studies (Sorbini et al. 1968) lay stress on the effects of posture on pulmonary gas exchange and on the falling Po2, especially in the supine posture, in ,elderly people. The importance of closure of gravitationally dependent airways in such hypoxamia in the elderly is now clearly understood (Craig et al. 1971, Collins 1973). On the normal basis of an arterial Pco2 which does not change much during life and an arterial Po2 which tends to fall with advancing years, disease imposes considerable variation. In the case of the arterial Po2, these are largely the result of alterations in the distribution of ventilation and blood flow within the lung. The effects of gravity on the distribution of ventilation have already been mentioned. In disease, dependent airway closure is of importance in obesity (Holley et al. 1967), in postoperative cases (Alexander et al. 1972), when the left atrial pressure is raised (Collins et al. 1972) and in hepatic cirrhosis (Ruff et al. 1971). Early disease of small airways in smokers may also affect airway closure (McCarthy etal. 1972). More marked impairment of distribution of ventilation and blood flow is frequently seen in lung disease and can be well analysed by the traditional method of determination of the deadspace:tidal volume ratio and the alveolararterial Po2 difference (Riley & Cournand 1951). In asthma, maldistribution of this type is a cause of the hypoxemia which persists into remission (Rees et al. 1968). It can be affected by bronchodilator drugs and by corticosteroids (EllulMicallef et al. 1972). The alterations in deadspace: tidal volume ratio and alveolar-arterial Po2 difference in bronchitis are well known (Jones 1966). However, it is of importance to realize that impaired distribution may be less noticeable at rest than during exercise both in established (Jones 1966) and early (Levine et al. 1970) disease. Hypercapnia is itself a cause of arterial hypoxaemia. It may be associated with severe derangement of pulmonary mechanics, as in chronic bronchitis, or may reflect a disturbance of the nervous control of breathing. Hypocapnia is found in thromboembolic pulmonary hypertension (Jones & Goodwin 1965) and in some forms of fibrosing alveolitis. Hypoximia due to veno-arterial shunting is an important factor in some types of congenital heart disease and may occur to a lesser extent in lung disease. It can be detected and quantified by various methods of which the most convenient in pulmonary disease is the breathing of 100% oxygen (Davidson et al. 1972). There remains the problem of hypoxwmia attributable to limitation of pulmonary diffusion. Although the calculations of Staub (1963) and the observations of Finley et al. (1962) made it seem unlikely that 'pure diffusion effects' could exist or contribute significantly to arterial hypoxaemia in disease, the situation is now being reappraised (McHardy 1972). It is possible under special circumstances to demonstrate hypoxwmia due to limitation of diffusion in normal subjects (Cohen et al. 1971). To demonstrate such limitation in disease requires complex techniques at present (Arndt et al. 1970), but it may be possible in future to provide a better distinction between the separate effects of impaired distribution and diffusion, particularly in fibrosing alveolitis.